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1. Antibody response against SARS-CoV-2 variants of concern in children infected with pre-Omicron variants: An observational cohort study

Author: Vanesa Seery, Silvina Raiden, Constanza Russo, Mauricio Borda, Largión Herrera, Macarena Uranga, Augusto Varese, María Marcó del Pont, Carina Chirino, Constanza Erramuspe, Laura Silvana Álvarez, Melisa Lenoir, Laura Daniela Morales, Carolina Davenport, Alexsa Alarcón Flores, Soledad Huespe Auchter, Yanina Ruiz, Liliana Monsalvo, Laura Sastoque, Magalí Gavazzi, Ignacio Mazzitelli, Facundo Di Diego, Yesica Longueira, Bianca Mazzitelli, Inés Sananez, Norberto De Carli, Mirna Marcela Biglione, Juan Martín Gómez Penedo, Ana Ceballos, Natalia Laufer, Fernando Ferrero, Jorge Geffner, and Lourdes Arruvito
Subjects: Pediatric COVID-19, SARS-CoV-2, Variants, Vaccines, Antibodies, Medicine, Medicine (General), R5-920
Abstract: Summary: Background: Despite that pediatric COVID-19 is usually asymptomatic or mild, SARS-CoV-2 infection typically results in the development of an antibody response. Contradictory observations have been reported when the antibody response of children and adults were compared in terms of strength, specificity and perdurability. Methods: This observational study includes three cohorts infected with SARS-CoV-2 between March 2020-July 2021: unvaccinated infected children (n=115), unvaccinated infected adults (n=62), and vaccinated infected children (n=76). Plasma anti-spike IgG antibodies and neutralising activity against Wuhan, Delta and Omicron variants after 7-17 months post-infection were analysed. Findings: More than 95% of unvaccinated infected children and adults remained seropositive when evaluated at 382-491 and 386-420 days after infection, respectively. Anti-spike IgG titers and plasma neutralising activity against Wuhan, Delta and Omicron variants were higher in children compared to adults. No differences were found when unvaccinated infected children were stratified by age, gender or presence/absence of symptoms in the acute phase of SARS-CoV-2 infection, but a slight decrease in the antibody response was observed in those with comorbidities. Vaccination of previously infected children with two doses of the inactivated BBIBP-CorV or the mRNA vaccines, BNT162b2 and/or mRNA-1273, further increased anti-spike IgG titers and neutralising activity against Wuhan, Delta and Omicron variants. Interpretation: Unvaccinated infected children mount a more potent and sustained antibody response compared with adults, which is significantly increased after vaccination. Further studies including not only the analysis of the immune response but also the effectiveness to prevent reinfections by the different Omicron lineages are required to optimise vaccination strategy in children. Funding: National Agency for Scientific and Technological Promotion from Argentina (PICTO-COVID-SECUELAS-00007 and PMO-BID-PICT2018-2548).
Published: 2022
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2. A poor and delayed anti-SARS-CoV2 IgG response is associated to severe COVID-19 in children

Author: Inés Sananez, Silvina C. Raiden, Silvia C. Algieri, Macarena Uranga, Nicolás A. Grisolía, Daniela Filippo, Norberto De Carli, Sandra Di Lalla, Héctor Cairoli, María J. Chiolo, Claudia N. Meregalli, Emilia Cohen, Graciela Mosquera, María Marcó del Pont, Lorena I. Giménez, Gabriela Gregorio, Mariam Sarli, Ana L. Alcalde, Carolina Davenport, María J. Bruera, Nancy Simaz, Mariela F. Pérez, Valeria Nivela, Carola Bayle, Laura Alvarez, María Revetria, Patricia Tuccillo, María T. Agosta, Hernán Pérez, Susana Villa Nova, Patricia Suárez, Eugenia M. Takata, Mariela García, Jorge Lattner, María J. Rolón, Patricia Coll, Melina Salvatori, Claudio Piccardo, Constanza Russo, Augusto Varese, Vanesa Seery, María P. Holgado, María L. Polo, Ana Ceballos, Myriam Nuñez, Juan Martín Gómez Penedo, Fernando Ferrero, Jorge Geffner, and Lourdes Arruvito
Subjects: Pediatric COVID-19, Disease severity, antibodies, T cells, Medicine, Medicine (General), R5-920
Abstract: Background: Most children and youth develop mild or asymptomatic disease during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, a very small number of patients suffer severe Coronavirus induced disease 2019 (COVID-19). The reasons underlying these different outcomes remain unknown. Methods: We analyzed three different cohorts: children with acute infection (n=550), convalescent children (n=138), and MIS-C (multisystem inflammatory syndrome in children, n=42). IgG and IgM antibodies to the spike protein of SARS-CoV-2, serum-neutralizing activity, plasma cytokine levels, and the frequency of circulating Follicular T helper cells (cTfh) and plasmablasts were analyzed by conventional methods. Findings: Fifty-eight percent of the children in the acute phase of infection had no detectable antibodies at the time of sampling while a seronegative status was found in 25% and 12% of convalescent and MIS-C children, respectively. When children in the acute phase of the infection were stratified according disease severity, we found that contrasting with the response of children with asymptomatic, mild and moderate disease, children with severe COVID-19 did not develop any detectable response. A defective antibody response was also observed in the convalescent cohort for children with severe disease at the time of admission. This poor antibody response was associated to both, a low frequency of cTfh and a high plasma concentration of inflammatory cytokines. Interpretation: A weak and delayed kinetic of antibody response to SARS-CoV-2 together with a systemic pro-inflammatory profile characterize pediatric severe COVID-19. Because comorbidities are highly prevalent in children with severe COVID-19, further studies are needed to clarify their contribution in the weak antibody response observed in severe disease. Funding: National Agency for Scientific and Technological Promotion from Argentina (IP-COVID-19-0277 and PMO-BID-PICT2018-2548).
Published: 2021
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3. Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers

Author: Vanesa Seery, Silvina C. Raiden, Silvia C. Algieri, Nicolás A. Grisolía, Daniela Filippo, Norberto De Carli, Sandra Di Lalla, Héctor Cairoli, María J. Chiolo, Claudia N. Meregalli, Lorena I. Gimenez, Gabriela Gregorio, Mariam Sarli, Ana L. Alcalde, Carolina Davenport, María J. Bruera, Nancy Simaz, Mariela F. Pérez, Valeria Nivela, Carola Bayle, Patricia Tuccillo, María T. Agosta, Hernán Pérez, Susana Villa Nova, Patricia Suárez, Eugenia M. Takata, Mariela García, Jorge Lattner, María J. Rolón, Patricia Coll, Inés Sananez, María P. Holgado, Fernando Ferrero, Jorge Geffner, and Lourdes Arruvito
Subjects: Pediatric COVID-19, Neutrophils, Fcγ receptor, Cell-adhesion molecules, Inhibitory Receptors, IgG, Medicine, Medicine (General), R5-920
Abstract: Background: Perhaps reflecting that children with COVID-19 rarely exhibit severe respiratory symptoms and often remain asymptomatic, little attention has been paid to explore the immune response in pediatric COVID-19. Here, we analyzed the phenotype and function of circulating neutrophils from children with COVID-19. Methods: An observational study including 182 children with COVID-19, 21 children with multisystem inflammatory syndrome (MIS-C), and 40 healthy children was performed in Buenos Aires, Argentina. Neutrophil phenotype was analyzed by flow cytometry in blood samples. Cytokine production, plasma levels of IgG antibodies directed to the spike protein of SARS-CoV-2 and citrullinated histone H3 were measured by ELISA. Cell-free DNA was quantified by fluorometry. Findings: Compared with healthy controls, neutrophils from children with COVID-19 showed a lower expression of CD11b, CD66b, and L-selectin but a higher expression of the activation markers HLA-DR, CD64 and PECAM-1 and the inhibitory receptors LAIR-1 and PD-L1. No differences in the production of cytokines and NETs were observed. Interestingly, the expression of CD64 in neutrophils and the serum concentration of IgG antibodies directed to the spike protein of SARS-CoV-2 distinguished asymptomatic from mild and moderate COVID-19. Interpretation: Acute lung injury is a prominent feature of severe COVID-19 in adults. A low expression of adhesion molecules together with a high expression of inhibitory receptors in neutrophils from children with COVID-19 might prevent tissue infiltration by neutrophils preserving lung function. Funding: This study was supported by the Ministry of Science and Technology (National Agency for Scientific and Technological Promotion, IP-COVID-19-0277 and PMO BID PICT 2018-2548), and University of Buenos Aires from Argentina (20020170100573BA).
Published: 2021
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4. Analysis of suppressor and non-suppressor FOXP3+ T cells in HIV-1-infected patients.

Author: Lourdes Arruvito, Juan Sabatté, Julieta Pandolfi, Plácida Baz, Luis A Billordo, Maria B Lasala, Horacio Salomón, Jorge Geffner, and Leonardo Fainboim
Subjects: Medicine, Science
Abstract: Recently, it was shown that peripheral blood FOXP3+CD4+ T cells are composed of three phenotypic and functionally distinct subpopulations. Two of them having in vitro suppressive effects were characterized as resting Treg cells (rTregs) and activated Treg cells (aTregs). A third subset, identified as FOXP3+ non-Tregs, does not display any suppressor activity and produce high levels of Th1 and Th17 cytokines upon stimulation. In the present study we focus on the characteristics of these three subsets of FOXP3+CD4+ T cells in untreated HIV-1-infected patients. We found that the absolute counts of rTregs, aTregs and FOXP3+ non-Tregs were reduced in HIV-1 patients compared with healthy donors. The relative frequency of rTregs and aTregs was similar in HIV-1 patients and healthy donors, while the frequency of FOXP3+ non-Tregs was significantly higher in HIV-1 patients, reaching a maximum in those patients with the lower values of CD4 counts. Contrasting with the observations made in FOXP3- CD4+ T cells, we did not find a negative correlation between the number of rTregs, aTregs or FOXP3+ non-Tregs and virus load. Studies performed with either whole PBMCs or sorted aTregs and FOXP3+ non-Tregs cells showed that these two populations of FOXP3+ T cells were highly permissive to HIV-1 infection. Upon infection, FOXP3+ non-Tregs markedly down-regulates its capacity to produce Th1 and Th17 cytokines, however, they retain the ability to produce substantial amounts of Th2 cytokines. This suggests that FOXP3+ non-Tregs might contribute to the polarization of CD4+ T cells into a Th2 profile, predictive of a poor outcome of HIV-1-infected patients.
Published: 2012
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5. Infants Younger Than 6 Months Infected With SARS-CoV-2 Show the Highest Respiratory Viral Loads

Author: Valeria, Ochoa, Fernando Erra, Díaz, Ezequiel, Ramirez, María Clara, Fentini, Mauricio, Carobene, Jorge, Geffner, Lourdes, Arruvito, Federico, Remes Lenicov, and Douglas, Vera Aguilar
Subjects: Pediatrics, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), CoV, viruses, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Respiratory System, Argentina, SARS-COV-2, purl.org/becyt/ford/3.3 [https], children, medicine, Humans, Immunology and Allergy, Respiratory system, COVID, SARS, SARS-CoV-2, business.industry, Brief Report, Infant, COVID-19, Viral Load, AcademicSubjects/MED00290, VIRAL LOAD, Infectious Diseases, purl.org/becyt/ford/3 [https], INFANT, business, Viral load
Abstract: There is a paucity of reports on the characteristics of SARS-CoV-2 infection in infants, since most studies have grouped infants with older children. We analyzed the viral loads of 45,318 SARS-CoV-2-positive nasopharyngeal swab samples obtained in Buenos Aires, Argentina. Infants younger than 6 months old presented higher viral loads than any other age group. Children older than 6 months showed significantly lower viral loads, similar to those founds in adults. This observation raises new questions regarding the role of infants in the spreading of SARS-CoV-2 infection. Fil: Ochoa, Valeria Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Erra Diaz, Fernando Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Ramirez, Joaquin Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Fentini, María Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Carobene, Mauricio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Published: 2021

6. Case Report: Relevance of an Accurate Diagnosis and Monitoring of Infective Dermatitis Associated With Human T-Lymphotropic Virus Type 1 in Childhood

Author: Magdalena Lamberti, Mirna M. Biglione, Nicolás Ducasa, Inés Irurzun, María Beraza, Laura Praino, Carolina Andrea Berini, Paula Benencio, and Lourdes Arruvito
Subjects: Medicine (General), medicine.medical_specialty, viruses, Argentina, Human T-lymphotropic virus, Myelopathy, R5-920, immune system diseases, antibiotic, hemic and lymphatic diseases, Tropical spastic paraparesis, medicine, case report, Risk factor, Tropism, biology, business.industry, infective dermatitis, virus diseases, General Medicine, medicine.disease, biology.organism_classification, Dermatology, Lymphoma, Leukemia, pediatric, medicine.anatomical_structure, HTLV-1, Scalp, Medicine, business
Abstract: Human T-lymphotropic virus type 1 (HTLV-1) is a neglected retrovirus distributed worldwide and the ethiological agent of several pathologies, such as adult T-cell leukemia/lymphoma (ATLL), a chronic myelopathy known as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and infective dermatitis associated with HTLV-1 (IDH). HTLV-1 presents tropism for CD4+ T cells and induces deregulation of the cytokine profile. IDH is a severe, chronic superinfected eczema generally associated with Staphylococcus aureus and/or Streptococcus beta haemolyticus infection that responds partially to antibiotic therapy but prompt recurrence develops upon treatment withdrawal. IDH could be a risk factor for progression toward both HAM/TSP and ATLL and, similarly to other diseases associated with HTLV-1, it is sub-diagnosed particularly in non-endemic areas. Here, we present a case of IDH in a young boy living in Buenos Aires with symptoms since 2010, at the age of 5. HTLV-1 infection was suspected and confirmed in 2016. The patient exhibited chronic dermatosis with exudative eruption involving mainly the scalp, retroauricular regions, neck and abdomen. Clinical evaluations, routine laboratory tests, full blood count, and HTLV-1 diagnosis for this case are included.
Published: 2021

7. A Poor and Delayed Anti-SARS-CoV2 IgG Response is Associated to Severe COVID-19 in Children

Author: Graciela Mosquera, Gabriela Gregorio, Maria Laura Polo, Claudia Meregalli, Laura Alvarez, Mariela García, María Marcó del Pont, María J. Chiolo, Susana Villa Nova, Maria Luisa Rolon, Inés Sananez, Macarena Uranga, Lourdes Arruvito, Patricia Tuccillo, Nicolás A. Grisolía, Jorge Lattner, Daniela Filippo, María Revetria, Melina Salvatori, Patricia Suárez, Silvia C. Algieri, María Pía Holgado, Ana L. Alcalde, Mariela F. Pérez, Valeria Nivela, Ana Ceballosa, María Temis Agosta, Patricia Coll, H. Cairoli, Eugenia M. Takata, María J. Bruera, Vanesa Seery, Nancy Simaz, Emilia Cohen, Carola Bayle, Fernando Ferrero, Sandra Di Lalla, Mariam Sarli, Jorge Geffner, Constanza Russo, Lorena I. Gimenez, Norberto De Carli, Hernán Pérez, Augusto Varese, Silvina Raiden, Claudio Piccardo, and Carolina Davenport
Subjects: Pediatrics, medicine.medical_specialty, biology, business.industry, Disease, Institutional review board, Asymptomatic, Informed consent, Informed assent, Cohort, biology.protein, Medicine, Sample collection, Antibody, medicine.symptom, business
Abstract: Background: Most children and youth develop mild or asymptomatic disease during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, a very small number of patients suffer severe Coronavirus induced disease 2019 (COVID-19). The reasons underlying these different outcomes remain unknown. Methods: We analyzed three different cohorts: children with acute infection (n=550), convalescent children (n=138), and MIS-C (multisystem inflammatory syndrome in children, n=42). IgG and IgM antibodies to the spike protein of SARS-CoV-2, serum-neutralizing activity, plasma cytokine levels, and the frequency of circulating Follicular T helper cells (cTfh) and plasmablasts were analyzed by conventional methods. Findings: Fifty-eight percent of the children in the acute phase of infection had no detectable antibodies at the time of sampling while a seronegative status was found in 25% and 12% of convalescent and MIS-C children, respectively. When children in the acute phase of the infection were stratified according disease severity, we found that contrasting with the response of children with asymptomatic, mild and moderate disease, children with severe COVID-19 did not develop any detectable response. A defective antibody response was also observed in the convalescent cohort for children with severe disease at the time of admission. This poor antibody response was associated to both, a low frequency of cTfh and a high plasma concentration of inflammatory cytokines. Interpretation: A weak and delayed kinetic of antibody response to SARS-CoV-2 together with a systemic pro-inflammatory profile characterize to pediatric severe COVID-19. Funding Information: National Agency for Scientific and Technological Promotion from Argentina (IP-COVID-19-0277 and PMO-BID-PICT2018-2548). Declaration of Interests: The authors have declared that no conflict of interest exists. Ethics Approval Statement: This study was conducted in accordance with the Declaration of Helsinki. The Institutional Review Board at institutions participants reviewed and approved the sample collection and the overall study (Hospital General de Ninos Pedro de Elizalde protocol reference 1226/20, Hospital Universitario Austral protocol reference 2147/2020 and Hospital General de Agudos Dr. J. A Fernandez protocol reference 1720/20). Parents or legal guardians from children under 8 years provided written, informed consent. Children older than 8 years old provided written, informed assent and their parents or legal guardians also provided written, informed consent.
Published: 2021

8. Fcγ Receptor IIa (FCGR2A) Polymorphism Is Associated With Severe Respiratory Syncytial Virus Disease in Argentinian Infants

Author: María Pía Holgado, Vanesa Seery, Lucas Luciano Maldonado, Jorge Geffner, Silvina Raiden, Leonardo De Lillo, Laura Kamenetzky, Inés Sananez, and Lourdes Arruvito
Subjects: 0301 basic medicine, Microbiology (medical), Immunology, lcsh:QR1-502, severity, Respiratory Syncytial Virus Infections, virus, Disease, FCGR2A, Microbiology, Fcγ receptor, lcsh:Microbiology, Virus, Pathogenesis, 03 medical and health sciences, Cellular and Infection Microbiology, 0302 clinical medicine, Immune system, Genotype, Humans, antibodies, Medicine, SNP, 030212 general & internal medicine, Child, Polymorphism, Genetic, biology, infants, business.industry, Receptors, IgG, Infant, Brief Research Report, Respiratory Syncytial Viruses, 030104 developmental biology, Infectious Diseases, biology.protein, Antibody, business
Abstract: BackgroundMost patients with respiratory syncytial virus (RSV) infection requiring hospitalization have no risk factors for severe disease. Genetic variation in the receptor for the Fc portion of IgG (FcγR) determines their affinity for IgG subclasses driving innate and adaptive antiviral immunity. We investigated the relationship between FcγRIIa-H131R polymorphism and RSV disease.MethodsBlood samples were collected from 182 infants ≤24-month-old (50 uninfected, 114 RSV-infected with moderate course and 18 suffering severe disease). FcγRIIa-H131R SNP genotypic frequencies (HH, HR, RR) and anti-RSV IgG1, IgG2 and IgG3 levels were studied.ResultsGenotypic frequencies for FcγRIIa-H131R SNP were comparable between uninfected and RSV-infected infants. In contrast, we found a significant higher frequency of HH genotype in severe RSV-infected children compared to moderate patients. Among severe group, HH infants presented more factors associated to severity than HR or RR patients did. Furthermore, compared to moderate RSV-infected infants, severe patients showed higher levels of anti-RSV IgG1 and IgG3.ConclusionsWe found an association between an FcγRIIa (H131) polymorphism and severe RSV disease, which points towards a critical role for interactions between FcγRs and immune complexes in RSV pathogenesis. This genetic factor could also predict the worse outcome and identify those infants at risk during hospitalization.
Published: 2020

9. Upregulation of CD32 in T Cells from Infants with Severe Respiratory Syncytial Virus Disease: A New Costimulatory Pathway?

Author: Leonardo De Lillo, Vanesa Seery, Inés Sananez, Silvina Raiden, Mark E. Peeples, Carolina Davenport, María Pía Holgado, Jorge Geffner, Fernando Ferrero, and Lourdes Arruvito
Subjects: Pulmonary and Respiratory Medicine, CD4-Positive T-Lymphocytes, Male, CD32, Clinical Biochemistry, CHILDREN, Respiratory Syncytial Virus Infections, Virus diseases, CD8-Positive T-Lymphocytes, FCGRII, Downregulation and upregulation, Correspondence, Medicine, Humans, Respiratory system, Receptor, Molecular Biology, biology, business.industry, Receptors, IgG, RSV, Infant, Cell Biology, purl.org/becyt/ford/3.1 [https], Respiratory Syncytial Viruses, Up-Regulation, T CELLS, Immunology, biology.protein, purl.org/becyt/ford/3 [https], Female, business
Abstract: Respiratory syncytial virus (RSV) causes 33.1 million episodes of acute lower respiratory infections, resulting in about 3.2 million hospital admissions, and 59 600 in-hospital deaths in children younger than 5 years during 2015, mostly in developing countries. An RSV-neutralizing monoclonal antibody (mAb), palivizumab, has been used prophylactically for 20 years for infants born prematurely or with heart malformations. The RSV vaccine candidates are evaluated based on their induction of RSV neutralizing Abs. However, antibodies can also influence the outcome of diseases by activating effector functions through the receptors for the Fc portion of IgG (FcRs). Whether T cell express FcRs is still controversial, but recent studies strongly suggest that a minor fraction of T cells expresses FcRII (CD32). Moreover, it should be noted that most severe RSV cases occur in infected infants under the age of 6 months, who are born with relatively high amounts of maternal IgG Ab to RSV. We here show that severe RSV infection in infants is associated with a marked upregulation of CD32 on T cells, whose ligation promotes the activation of CD4+ and CD8+ T cells of hospitalized infants. These findings also suggest that during severe RSV infection in infants, the immune complexes might provide a stimulatory signal able to promote the activation of T cells contributing to the resolution of infection. Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Seery, Vanesa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Davenport, Carolina. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Ferrero, Fernando. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Peeples, Mark E.. No especifíca; Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Published: 2020

10. A poor and delayed anti-SARS-CoV2 IgG response is associated to severe COVID-19 in children

Author: María Marcó del Pont, Lorena I. Gimenez, Norberto De Carli, Maria Laura Polo, Laura Alvarez, Melina Salvatori, Jorge Geffner, Augusto Varese, Juan Martín Gómez Penedo, Silvina Raiden, Eugenia M. Takata, María Revetria, Ana L. Alcalde, María Temis Agosta, Patricia Coll, Hernán Pérez, Macarena Uranga, Nancy Simaz, Constanza Russo, Mariela García, Patricia G Suárez, Ana Ceballos, Carola Bayle, Fernando Ferrero, María J. Chiolo, Susana Villa Nova, María José Rolón, Lourdes Arruvito, Héctor Cairoli, Mariam Sarli, Sandra Di Lalla, Inés Sananez, Emilia Cohen, Graciela Mosquera, Gabriela Gregorio, Jorge Lattner, Nicolás A. Grisolía, Claudia Meregalli, María J. Bruera, María P. Holgado, Silvia C. Algieri, Mariela F. Pérez, Valeria Nivela, Vanesa Seery, Claudio Piccardo, Patricia Tuccillo, Daniela Filippo, Myriam Nuñez, and Carolina Davenport
Subjects: Male, Medicine (General), Disease severity, antibodies, T cells, Argentina, Disease, Antibodies, Viral, medicine.disease_cause, Asymptomatic, General Biochemistry, Genetics and Molecular Biology, Immunoglobulin G, R5-920, Humans, Medicine, Child, Coronavirus, biology, SARS-CoV-2, business.industry, COVID-19, Infant, General Medicine, medicine.disease, Systemic Inflammatory Response Syndrome, Pediatric COVID-19, Systemic inflammatory response syndrome, Immunoglobulin M, Child, Preschool, Antibody Formation, Immunology, Cohort, biology.protein, Cytokines, Female, medicine.symptom, Antibody, business, Research Paper
Abstract: Background Most children and youth develop mild or asymptomatic disease during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, a very small number of patients suffer severe Coronavirus induced disease 2019 (COVID-19). The reasons underlying these different outcomes remain unknown. Methods We analyzed three different cohorts: children with acute infection (n=550), convalescent children (n=138), and MIS-C (multisystem inflammatory syndrome in children, n=42). IgG and IgM antibodies to the spike protein of SARS-CoV-2, serum-neutralizing activity, plasma cytokine levels, and the frequency of circulating Follicular T helper cells (cTfh) and plasmablasts were analyzed by conventional methods. Findings Fifty-eight percent of the children in the acute phase of infection had no detectable antibodies at the time of sampling while a seronegative status was found in 25% and 12% of convalescent and MIS-C children, respectively. When children in the acute phase of the infection were stratified according disease severity, we found that contrasting with the response of children with asymptomatic, mild and moderate disease, children with severe COVID-19 did not develop any detectable response. A defective antibody response was also observed in the convalescent cohort for children with severe disease at the time of admission. This poor antibody response was associated to both, a low frequency of cTfh and a high plasma concentration of inflammatory cytokines. Interpretation A weak and delayed kinetic of antibody response to SARS-CoV-2 together with a systemic pro-inflammatory profile characterize pediatric severe COVID-19. Because comorbidities are highly prevalent in children with severe COVID-19, further studies are needed to clarify their contribution in the weak antibody response observed in severe disease. Funding National Agency for Scientific and Technological Promotion from Argentina (IP-COVID-19-0277 and PMO-BID-PICT2018-2548).
Published: 2021

11. Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers

Author: Lorena I. Gimenez, Claudia Meregalli, Norberto De Carli, María J. Chiolo, Susana Villa Nova, Mariela García, María P. Holgado, Jorge Lattner, María José Rolón, Hernán Pérez, Silvia C. Algieri, Nicolás A. Grisolía, Eugenia M. Takata, Mariam Sarli, María J. Bruera, Mariela F. Pérez, Valeria Nivela, Sandra Di Lalla, Patricia G Suárez, Silvina Raiden, Nancy Simaz, Patricia Tuccillo, Carola Bayle, Fernando Ferrero, Inés Sananez, Jorge Geffner, Daniela Filippo, Ana L. Alcalde, Carolina Davenport, María Temis Agosta, Patricia Coll, Vanesa Seery, Gabriela Gregorio, Lourdes Arruvito, and Héctor Cairoli
Subjects: 0301 basic medicine, Male, Medicine (General), Neutrophils, medicine.medical_treatment, Antibodies, Viral, Immunoglobulin G, Fcγ receptor, 0302 clinical medicine, Child, NEUTROPHILS, CD64, biology, PEDIATRIC COVID-19, purl.org/becyt/ford/3.1 [https], General Medicine, Flow Cytometry, Systemic Inflammatory Response Syndrome, Pediatric COVID-19, Cytokine, Integrin alpha M, 030220 oncology & carcinogenesis, Child, Preschool, Spike Glycoprotein, Coronavirus, CELL-ADHESION MOLECULES, Medicine, Cytokines, purl.org/becyt/ford/3 [https], Female, Sample collection, Antibody, medicine.symptom, Inhibitory Receptors, Selectin, Research Paper, Cell-adhesion molecules, IgG, Argentina, Lung injury, Asymptomatic, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Immune system, R5-920, medicine, Humans, IGG, business.industry, SARS-CoV-2, INHIBITORY RECEPTORS, COVID-19, Infant, medicine.disease, FCΓ RECEPTOR, Systemic inflammatory response syndrome, 030104 developmental biology, Case-Control Studies, Immunology, biology.protein, business, Biomarkers
Abstract: Background: Perhaps reflecting that children with COVID-19 rarely exhibit severe respiratory symptoms and often remain asymptomatic, little attention has been paid to explore the immune response in pediatric COVID-19. Here, we analyzed the phenotype and function of circulating neutrophils from children with COVID-19. Methods: An observational study including 182 children with COVID-19, 21 children with multisystem inflammatory syndrome (MIS-C), and 40 healthy children was performed in Buenos Aires, Argentina. Neutrophil phenotype was analyzed by flow cytometry in blood samples. Cytokine production, plasma levels of IgG antibodies directed to the spike protein of SARS-CoV-2 and citrullinated histone H3 were measured by ELISA. Cell-free DNA was quantified by fluorometry. Findings: Compared with healthy controls, neutrophils from children with COVID-19 showed a lower expression of CD11b, CD66b, and L-selectin but a higher expression of the activation markers HLA-DR, CD64 and PECAM-1 and the inhibitory receptors LAIR-1 and PD-L1. No differences in the production of cytokines and NETs were observed. Interestingly, the expression of CD64 in neutrophils and the serum concentration of IgG antibodies directed to the spike protein of SARS-CoV-2 distinguished asymptomatic from mild and moderate COVID-19. Interpretation: Acute lung injury is a prominent feature of severe COVID-19 in adults. A low expression of adhesion molecules together with a high expression of inhibitory receptors in neutrophils from children with COVID-19 might prevent tissue infiltration by neutrophils preserving lung function. Fil: Seery, Vanesa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Algieri, Silvia C.. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Grisolía, Nicolás A.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Filippo, Daniela. Hospital Municipal Diego Thompson; Argentina Fil: De Carli, Norberto. Clinica del Niño de Quilmes; Argentina Fil: Di Lalla, Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Cairoli, Héctor. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Chiolo, María J.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Meregalli, Claudia N.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Gimenez, Lorena I.. Hospital Municipal Diego Thompson; Argentina Fil: Gregorio, Gabriela. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Sarli, Mariam. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Alcalde, Ana L.. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Davenport, Carolina. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Bruera, María J.. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Simaz, Nancy. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Pérez, Mariela F.. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Nivela, Valeria. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Bayle, Carola. Hospital Nacional Profesor Alejandro Posadas.; Argentina Fil: Tuccillo, Patricia. Ministerio de Defensa. Armada Argentina. Hospital Naval Buenos Aires Cirujano Mayor Dr. Pedro Mallo; Argentina Fil: Agosta, María T.. Ministerio de Defensa. Armada Argentina. Hospital Naval Buenos Aires Cirujano Mayor Dr. Pedro Mallo; Argentina Fil: Pérez, Hernán. Ministerio de Defensa. Armada Argentina. Hospital Naval Buenos Aires Cirujano Mayor Dr. Pedro Mallo; Argentina Fil: Villa Nova, Susana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Suárez, Patricia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Takata, Eugenia M.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: García, Mariela. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Lattner, Jorge. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Rolón, María J.. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Coll, Patricia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Juan A. Fernández"; Argentina Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Ferrero, Fernando. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Published: 2021

12. CD32 ligation promotes the activation of CD4+T cells

Author: María Pía Holgado, Inés Sananez, Silvina Raiden, Jorge R. Geffner, and Lourdes Arruvito
Subjects: 0301 basic medicine, lcsh:Immunologic diseases. Allergy, CD32, CIENCIAS MÉDICAS Y DE LA SALUD, medicine.drug_class, IgG, proliferation, Immunology, Cell, Fc receptor, T cells, Inmunología, Monoclonal antibody, ACTIVATION, 03 medical and health sciences, 0302 clinical medicine, Immune system, FcγR, medicine, Immunology and Allergy, Receptor, biology, Chemistry, IGG, CYTOKINES, FCΓR, PROLIFERATION, purl.org/becyt/ford/3.1 [https], Acquired immune system, Molecular biology, cytokines, Medicina Básica, 030104 developmental biology, medicine.anatomical_structure, Cytoplasm, 030220 oncology & carcinogenesis, T CELLS, biology.protein, activation, purl.org/becyt/ford/3 [https], lcsh:RC581-607
Abstract: Low affinity receptors for the Fc portion of IgG (FcγRs) represent a critical link between innate and adaptive immunity. Immune complexes (ICs) are the natural ligands for low affinity FcγRs, and high levels of ICs are usually detected in both, chronic viral infections and autoimmune diseases. The expression and function of FcγRs in myeloid cells, NK cells and B cells have been well characterized. By contrast, there are controversial reports about the expression and function of FcγRs in T cells. Here, we demonstrated that ∼2% of resting CD4+ T cells express cell surface FcγRII (CD32). Analysis of CD32 expression in permeabilized cells revealed an increased proportion of CD4+CD32+ T cells (∼9%), indicating that CD4+ T cells store a CD32 cytoplasmic pool. Activation of CD4+ T cells markedly increased the expression of CD32 either at the cell surface or intracellularly. Analysis of CD32 mRNA transcripts in activated CD4+ T cells revealed the presence of both, the stimulatory FcγRIIa (CD32a) and the inhibitory FcγRIIb (CD32b) isoforms of CD32, being the CD32a:CD32b mRNA ratio ∼5:1. Consistent with this finding, we found not only that CD4+ T cells bind aggregated IgG, used as an IC model, but also that CD32 ligation by specific mAb induced a strong calcium transient in CD4+ T cells. Moreover, we found that pretreatment of CD4+ T cells with immobilized IgG as well as cross-linking of CD32 by specific antibodies increased both, the proliferative response of CD4+ T cells and the release of a wide pattern of cytokines (IL-2, IL-5, IL-10, IL-17, IFN-γ, and TNF-α) triggered by either PHA or anti-CD3 mAb. Collectively, our results indicate that ligation of CD32 promotes the activation of CD4+ T cells. These findings suggest that ICs might contribute to the perpetuation of chronic inflammatory responses by virtue of its ability to directly interact with CD4+ T cells through CD32a, promoting the activation of T cells into different inflammatory profiles. Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Published: 2018

13. Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease

Author: Fernando Erra-Díaz, Leonardo De Lillo, María Pía Holgado, Jorge Geffner, Silvina Raiden, Inés Sananez, and Lourdes Arruvito
Subjects: 0301 basic medicine, Male, CIENCIAS MÉDICAS Y DE LA SALUD, FOXP3, Inmunología, RESPIRATORY SYNCYTIAL VIRUS, INFANTS, Enzyme-Linked Immunosorbent Assay, Respiratory Syncytial Virus Infections, Virus diseases, SEVERE BRONCHIOLITIS, T-Lymphocytes, Regulatory, 03 medical and health sciences, 0302 clinical medicine, Immunology and Allergy, Medicine, Humans, Immunologic Factors, Respiratory system, CD25, business.industry, IL-2, Interleukin-2 Receptor alpha Subunit, Infant, purl.org/becyt/ford/3.1 [https], Flow Cytometry, Virology, CD4 + T CELLS, FOXP3 gene, Medicina Básica, 030104 developmental biology, Infectious Diseases, Interleukin-2, Female, purl.org/becyt/ford/3 [https], business, 030215 immunology
Abstract: Background FOXP3 + regulatory T cells (Tregs) restrain the destructive potential of the immune system. We have previously reported a pronounced reduction in circulating Tregs in infants with severe respiratory syncytial virus (RSV) disease. Because interleukin-2 (IL-2) is critical for Treg growth, survival, and activity, we here analyzed IL-2 production and function in RSV-infected infants. Methods Phenotype, proliferation, IL-2 production, and IL-2 signaling in CD4 + T cells were analyzed by flow cytometry. Serum soluble CD25 levels were quantified by ELISA. Results CD4 + T cells from RSV-infected infants produced lower amounts of IL-2 and showed a reduced proliferative response compared with healthy infants. IL-2 increased CD4 + T-cell proliferation and FOXP3 expression in both healthy and RSV-infected infants. However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4 + T cells and the expression of FOXP3 + remained significantly lower in RSV-infected infants. Interestingly, we found a negative correlation between disease severity and both the production of IL-2 by CD4 + T cells and the ability of exogenous IL-2 to restore the pool of FOXP3 + CD4 + T cells. Conclusions A reduced ability to produce IL-2 and a limited response to this cytokine may affect the function of CD4 + T cells in RSV-infected infants. Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Erra Diaz, Fernando Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Holgado, María Pía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Published: 2018

14. Host response to respiratory syncytial virus infection

Author: Jorge Geffner, Lourdes Arruvito, and Silvina Raiden
Subjects: Microbiology (medical), viruses, Host response, Respiratory Syncytial Virus Infections, Adaptive Immunity, T-Lymphocytes, Regulatory, Virus, Mice, Immune system, Immunity, Respiratory Syncytial Virus Vaccines, Animals, Humans, Medicine, Respiratory system, business.industry, Infant, Acquired immune system, medicine.disease, Virology, Immunity, Innate, Respiratory Syncytial Viruses, Disease Models, Animal, Infectious Diseases, Bronchiolitis, Host-Pathogen Interactions, Immunology, Bronchitis, business
Abstract: Respiratory syncytial virus (RSV) infection is the leading cause of bronchiolitis and hospitalization in young infants and causes 100, 000-200, 000 deaths annually. There is still no licensed vaccine against RSV infection and the therapeutic options are mainly supportive. Despite almost six decades of research, important knowledge gaps remain with respect to the characterization of immune mechanisms responsible for protection and pathogenesis, as well as to the identification of risk factors that predict the severity of infection.Observations made in mouse models and young children suggest that the early innate immune response plays a major role in the pathogenesis of bronchiolitis due to RSV infection. Recent studies have improved our understanding of the role of the adaptive immune response mediated by TH1, TH2, TH17, regulatory T cells, and CD8 T cells in the pathogenesis and resolution of RSV infection. Moreover, investigations performed in the last years have made important contributions to our knowledge of the immune response in young children, the principal risk group for severe disease.A comprehensive understanding of how the protective and deleterious immune response during the course of RSV infection is induced in young children remains a challenge over the coming years.
Published: 2015

15. Purinergic signaling modulates human visceral adipose inflammatory responses: implications in metabolically unhealthy obesity

Author: Leonardo Fainboim, A. Dueck, Julieta Pandolfi, M. Lerner, Lourdes Arruvito, Ariel Ferraro, and J.R. Serrano
Subjects: medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Adenosine, Immunology, Inmunología, Inflammation, Biology, Proinflammatory cytokine, ATP hydrolysis, Internal medicine, medicine, Immunology and Allergy, Purinergic receptor, Inflammasome, purl.org/becyt/ford/3.1 [https], Cell Biology, Purinergic signalling, Atp, Medicina Básica, Endocrinology, purl.org/becyt/ford/3 [https], medicine.symptom, Signal transduction, medicine.drug
Abstract: Obesity is accompanied by chronic inflammation of VAT, which promotes metabolic changes, and purinergic signaling has a key role in a wide range of inflammatory diseases. Therefore, we addressed whether fat inflammation could be differentially modulated by this signaling pathway in the MUO and in individuals who remain MHO. Our results show that the necrotized VAT of both groups released greater levels of ATP compared with lean donors. Interestingly, MUO tissue SVCs showed up-regulation and engagement of the purinergic P2X7R. The extracellular ATP concentration is regulated by an enzymatic process, in which CD39 converts ATP and ADP into AMP, and CD73 converts AMP into adenosine. In VAT, the CD73 ectoenzyme was widely distributed in immune and nonimmune cells, whereas CD39 expression was restricted to immune CD45PAN+ SVCs. Although the MUO group expressed the highest levels of both ectoenzymes, no difference in ATP hydrolysis capacity was found between the groups. As expected, MUO exhibited the highest NLRP3 inflammasome expression and IL-1β production. MUO SVCs also displayed up-regulation of the A2AR, allowing extracellular adenosine to increase IL-1β local secretion. Additionally, we demonstrate that metabolic parameters and BMI are positively correlated with purinergic components in VAT. These findings indicate that purinergic signaling is a novel mechanism involved in the chronic inflammation of VAT underlying the metabolic changes in obesity. Finally, our study reveals a proinflammatory role for adenosine in sustaining IL-1β production in this tissue. Fil: Pandolfi, Julieta Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Ferraro, A.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Lerner, M.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Serrano, J. R.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Dueck, A.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Published: 2015

16. Identification and Clinical Relevance of Naturally Occurring Human CD8+HLA-DR+ Regulatory T Cells

Author: Plácida Baz, Guillermo B. Semeniuk, Ariel Podhorzer, Leonardo Fainboim, Eduardo B Arribalzaga, Lourdes Arruvito, Julieta Pandolfi, Ariel Billordo, and Florencia Payaslian
Subjects: Male, Respuesta Inmune, Cell signaling, CIENCIAS MÉDICAS Y DE LA SALUD, Regulatory T cell, T cell, Immunology, Inmunología, Cell Communication, CD8-Positive T-Lymphocytes, Biology, Lymphocyte Activation, T-Lymphocytes, Regulatory, Peripheral blood mononuclear cell, Immunophenotyping, Immunomodulation, Interleukin 21, T-Lymphocyte Subsets, Carcinoma, Non-Small-Cell Lung, medicine, HLA-DR, Humans, Immunology and Allergy, CTLA-4 Antigen, Lymphocyte Count, Aged, Cell Proliferation, Aged, 80 and over, Celulas T regulatorias, Infant, Newborn, HLA-DR Antigens, Middle Aged, Fetal Blood, Medicina Básica, Phenotype, medicine.anatomical_structure, Leukocytes, Mononuclear, Cancer research, Interleukin-2, Female, Cáncer de Pulmon, CD8
Abstract: The lack of responsiveness to self and non-self Ags is normally maintained by multiple mechanisms, including the suppressive activities of several T cell subsets. In this study, we show that CD8+ T cells from both adult peripheral blood and umbilical cord blood mononuclear cells constitutively expressing HLA-DR represent a natural human CD8+ regulatory T cell subset. Their suppressive effect appears to be cell-to-cell contact dependent and may involve CTLA-4 signaling between neighboring T cells. These regulatory T cells can be expanded in vitro and exhibit a suppressive capacity similar to that observed in ex vivo CD8+HLA-DR+ T cells. The high frequency of CD8+HLA-DR+ T cells that we detected in patients with non–small cell lung cancer deserves further work to confirm their putative suppressor effect within the tumor. Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Payaslián, Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Podhorzer, Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Billordo, Luis Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Pandolfi, Julieta Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Semeniuk, Guillermo Basilio. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina Fil: Arribalzaga, Eduardo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Published: 2014

17. Respiratory Syncytial Virus (RSV) Infects CD4+ T Cells: Frequency of Circulating CD4+ RSV+ T Cells as a Marker of Disease Severity in Young Children

Author: Cecilia Romero, Silvina Raiden, Leonardo De Lillo, Federico Remes-Lenicov, Jorge Geffner, Ana Ceballos, Julieta Pandolfi, Inés Sananez, and Lourdes Arruvito
Subjects: CD4-Positive T-Lymphocytes, Male, 0301 basic medicine, viruses, medicine.medical_treatment, CD8-Positive T-Lymphocytes, Respiratory syncytial virus, medicine.disease_cause, Interleukin 2, Interferon γ, 0302 clinical medicine, Immunology and Allergy, IL-2 receptor, purl.org/becyt/ford/3.1 [https], Fetal Blood, Flow Cytometry, Medicina Básica, Infectious Diseases, Respiratory syncytial virus (RSV), Cytokine, Bronchiolitis, purl.org/becyt/ford/3 [https], Female, Infants, medicine.drug, Adult, CIENCIAS MÉDICAS Y DE LA SALUD, Inmunología, Respiratory Syncytial Virus Infections, Biology, Virus, Cell Line, Interferon-gamma, 03 medical and health sciences, Immune system, Antigen, Markers of disease severity, Major Article, medicine, Humans, Infant, Newborn, Infant, Virology, CD4+ T cells, 030104 developmental biology, Viral infection, Respiratory Syncytial Virus, Human, Interleukin-2, Biomarkers, CD8, 030215 immunology
Abstract: Background: Although human airway epithelial cells are the main target of respiratory syncytial virus (RSV), it also infects immune cells, such as macrophages and B cells. Whether T cells are permissive to RSV infection is unknown. We sought to analyze the permissiveness of CD4+ T cells to RSV infection. Methods: CD4+ and CD8+ T cells from cord blood, healthy young children, and adults were challenged by RSV or cocultured with infected HEp-2 cells. Infection, phenotype, and cytokine production by T cells were analyzed by flow cytometry or enzymelinked immunosorbent assay. Expression of RSV antigens by circulating CD4+ T cells from infected children was analyzed by flow cytometry, and disease severity was defined by standard criteria. Results: CD4+ and CD8+ T cells were productively infected by RSV. Infection decreased interleukin 2 and interferon γ production as well as the expression of CD25 and Ki-67 by activated CD4+ T cells. Respiratory syncytial virus antigens were detected in circulating CD4+ and CD8+ T cells during severe RSV infection of young children. Interestingly, the frequency of CD4+ RSV+ T cells positively correlated with disease severity. Conclusions: Respiratory syncytial virus infects CD4+ and CD8+ T cells and compromises T-cell function. The frequency of circulating CD4+ RSV+ T cells might represent a novel marker of severe infection. Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina Fil: Pandolfi, Julieta Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Romero, Cecilia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Ceballos, Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Published: 2017

18. Regulatory and effector T-cells are differentially modulated by Dexamethasone

Author: Julieta Pandolfi, Florencia Payaslian, Pablo M. Fernández, Leonardo Fainboim, Lourdes Arruvito, Plácida Baz, Ailén Discianni Lupi, and Luis Ariel Billordo
Subjects: Adult, Male, Interleukin 2, endocrine system, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Cell Survival, Immunology, Inmunología, Anti-Inflammatory Agents, Gene Expression, Apoptosis, chemical and pharmacologic phenomena, Biology, Lymphocyte Activation, T-Lymphocytes, Regulatory, Dexamethasone, REGULATORY T CELLS, Glucocorticoid receptor, EFFECTOR T CELLS, Internal medicine, polycyclic compounds, medicine, Homeostasis, Humans, Immunology and Allergy, GLUCOCORTICOIDS, IL-2 receptor, Antigen-presenting cell, Cell Proliferation, Cell growth, CYTOKINES, Interleukin-2 Receptor alpha Subunit, FOXP3, Forkhead Transcription Factors, hemic and immune systems, APOPTOSIS, DEXAMETHASONE, Cell biology, Medicina Básica, Endocrinology, Organ Specificity, Interleukin-2, Female, hormones, hormone substitutes, and hormone antagonists, T-Lymphocytes, Cytotoxic, medicine.drug
Abstract: It is assumed that the ratio between effector T cells (Teff) and regulatory T cells (Tregs) controls the immune reactivity within the T-cell compartment. The purpose of this study was to investigate if Dexamethasone (Dex) affects Teff and Tregs subsets. Dex induced on Tregs a dose and time-dependent apoptosis which resulted in a relative increase of Teff. After TCR activation, Dex induced a strong proliferative inhibition of Teff, but a weaker proliferative inhibition on Tregs. These effects were modulated by IL-2, which not only restored the proliferative response, but also prevented Dex-induced apoptosis. The highest dose of IL-2 prevented apoptosis on all FOXP3 + CD4+ T cells. Meanwhile, the lowest dose only rescued activated Tregs (aTregs), probably related to their CD25 higher expression. Because Dex did not affect the suppressor capacity of aTregs either, our results support the notion that under Dex treatment, the regulatory T-cell compartmentmaintains its homeostasis. Fil: Pandolfi, Julieta Belen. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Fil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Fil: Fernandez, Pablo Mariano. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Fil: Discianni Lupi, Ailen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina; Fil: Payaslián, Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Fil: Billordo, Luis Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina; Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo; Argentina; Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Published: 2013

19. Expansion of CD4+CD25+and FOXP3+ regulatory T cells during the follicular phase of the menstrual cycle: implications for human reproduction

Author: Lourdes Arruvito, Marianela Sanz, Leonardo Fainboim, and Alison H. Banham
Subjects: Adult, Male, medicine.medical_specialty, Abortion, Habitual, CIENCIAS MÉDICAS Y DE LA SALUD, FOXP3, media_common.quotation_subject, Immunology, Inmunología, chemical and pharmacologic phenomena, Luteal phase, Biology, Luteal Phase, T-Lymphocytes, Regulatory, Autoimmune Diseases, REGULATORY T CELLS, Pregnancy, Internal medicine, Follicular phase, medicine, Immunology and Allergy, Humans, IL-2 receptor, Menstrual cycle, media_common, Aged, Autoimmune disease, Estradiol, hemic and immune systems, Forkhead Transcription Factors, purl.org/becyt/ford/3.1 [https], Middle Aged, medicine.disease, Postmenopause, Medicina Básica, Endocrinology, Follicular Phase, purl.org/becyt/ford/3 [https], Female, Hormone
Abstract: Regulatory T cells (Tregs) are thought to affect the severity of various infectious and autoimmune diseases. The incidence of autoimmune disease is higher in fertile women than in men. Thus, we investigated whether Treg numbers were modulated during the menstrual cycle by sex hormones. In fertile nonpregnant women, we detected an expansion of CD4 CD25 FOXP3 Tregs in the late follicular phase of the menstrual cycle. This increase was tightly correlated with serum levels of estradiol and was followed by a dramatic decrease in Treg numbers at the luteal phase. Women who have had recurrent spontaneous abortions (RSA) showed similarly low numbers of Tregs at both the follicular and luteal phases, comparable to numbers we observed in postmenopausal women. In addition to decreased numbers, Tregs from women with RSA were also functionally deficient, as higher numbers were required to exert a similar magnitude of suppression to CD4 CD25 FOXP3 cells from fertile women. Consequently, reproductive failure might result from the inability of Tregs in women with RSA to expand during the preimplantatory phase combined with their lower functional capacity. Additionally, the modulation of Treg numbers we observed in fertile women suggests that the stage of the menstrual cycle should be taken into account when Treg numbers are investigated clinically. The Journal of Immunology, 2007, 178: 2572–2578. Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Sanz, Marianela. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Banham, Alison H.. University of Oxford; Reino Unido Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Published: 2016

20. ATP-Induced Inflammation Drives Tissue-Resident Th17 Cells in Metabolically Unhealthy Obesity

Author: Ariel Ferraro, Lourdes Arruvito, Leonardo Fainboim, Inés Sananez, Plácida Baz, Julieta Pandolfi, Maria C. Gancedo, and Luis Ariel Billordo
Subjects: 0301 basic medicine, Adult, Male, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, medicine.medical_treatment, T cell, Immunology, Interleukin-1beta, Inmunología, Adipose tissue, Inflammation, Apoptosis, Biology, Intra-Abdominal Fat, 03 medical and health sciences, 0302 clinical medicine, Immune system, Adenosine Triphosphate, INFLAMMATION, RAR-related orphan receptor gamma, Antigens, CD, Internal medicine, medicine, Immunology and Allergy, Humans, TH17, Obesity, Receptor, Interleukin-6, Apyrase, Interleukin-17, Receptors, Interleukin, Purinergic signalling, Nuclear Receptor Subfamily 1, Group F, Member 3, ATP, Medicina Básica, 030104 developmental biology, Cytokine, Endocrinology, medicine.anatomical_structure, Cellular Microenvironment, OBESITY, Th17 Cells, Female, Receptors, Purinergic P2X7, medicine.symptom, 030215 immunology
Abstract: Obesity-induced inflammation is conducted by a metabolic pathway, which eventually causes activation of specialized immune cells and leads to an unresolved inflammatory response within the tissue. For this reason, it is critically important to determine how hypertrophic fat tissue alters T cell balance to drive inflammation. In this study, we identify the purinergic signaling as a novel mechanism driving the adaptive Th17 response in human visceral adipose tissue (VAT) of metabolically unhealthy obese patients. We demonstrate that ATP acting via the P2X7 receptor pathway promotes a Th17 polarizing microenvironment with high levels of IL-1β, IL-6, and IL-17 in VAT explants from lean donors. Moreover, in vitro blockade of the P2X7 receptor abrogates the levels of these cytokines. These findings are consistent with a greater frequency of Th17 cells in tissue from metabolically unhealthy obese donors, revealed not only by the presence of a baseline Th17-promoting milieu, but also by the higher expression of steadily recognized Th17 markers, such as RORC, IL-17 cytokine, and IL-23R, in comparison with metabolically healthy obese and lean donors. In addition, we demonstrate that CD39 expression on CD4+ effector T cells represents a novel Th17 marker in the inflamed VAT, which also confers protection against ATP-induced cell death. The manipulation of the purinergic signaling might represent a new therapeutic target to shift the CD4+ T cell balance under inflammatory conditions. Fil: Pandolfi, Julieta Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Ferraro, Sebastián Ariel. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Sananez, Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Gancedo, Maria Clotilde. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Billordo, Luis Ariel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Published: 2015

21. A physiological role for inducible FOXP3+ TREG cells

Author: Lourdes Arruvito, Leonardo Fainboim, Ariel Billordo, and Ana I. Sotelo
Subjects: business.industry, Immunology, Lymphocyte activation, Immunology and Allergy, Medicine, business, Humanities, Treg cell, Interleukine 2, Reproductive failure
Abstract: Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clinicas General San Martin; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiologia. Catedra de Microbiologia, Parasitologia e Inmunologia; Argentina
Published: 2010

22. Cytokines and chronic liver disease

Author: Natalia Paladino, Leonardo Fainboim, Ana C. Flores, Lourdes Arruvito, and Alejandra C. Cherñavsky
Subjects: Kupffer Cells, Endocrinology, Diabetes and Metabolism, Immunology, Biology, Chronic liver disease, Autoantigens, General Biochemistry, Genetics and Molecular Biology, Immune tolerance, Immune Tolerance, medicine, Animals, Humans, Immunology and Allergy, Hepatovirus, Pathological, Liver immunology, Liver injury, Hepatitis, Liver Diseases, Endothelial Cells, Dendritic Cells, medicine.disease, Chronic disease, Liver, Organ Specificity, Chronic Disease, Cytokines, Liver pathology
Abstract: From an immunological point of view, the healthy liver has been usually associated with the phenomenon of tolerance. A microenvironment of regulatory cytokines produced by liver Kuppfer cells and liver sinusoidal endothelial cells has contributed, together with resident dendritic cells, to generate a tolerogenic environment in this tissue. In this review we discussed the intrahepatic responses to different sorts of liver injury, such as hepatotrophic viruses, alcohol or putative self-antigens. In each case we analyzed the impact of different cytokines in the clinical outcome of the different pathological situations.
Published: 2007

23. Mechanisms involved in the expansion of Tregs during pregnancy: Role of IL-2/STAT5 signalling

Author: Leonardo Fainboim and Lourdes Arruvito
Subjects: Interleukin 2, CIENCIAS MÉDICAS Y DE LA SALUD, Regulatory T cell, medicine.medical_treatment, Immunology, Inmunología, T-Lymphocytes, Regulatory, HUMAN REPRODUCTION, Immune tolerance, Pregnancy, medicine, Immune Tolerance, STAT5 Transcription Factor, Immunology and Allergy, Endocrine system, Animals, Humans, Gonadal Steroid Hormones, STAT5, Cell Proliferation, REGULATORY T CELL, biology, IL-2, Obstetrics and Gynecology, FOXP3, medicine.disease, Pregnancy Complications, Medicina Básica, medicine.anatomical_structure, Cytokine, Reproductive Medicine, biology.protein, Interleukin-2, Female, STAT-5, medicine.drug, Signal Transduction
Abstract: Several studies have reported that the fine-tuning of regulatory T cells (Tregs) is required for a successful pregnancy and for the control of autoimmune diseases. Here, we review the mechanisms that control the expansion of Tregs, based on insights obtained from the study of women suffering unsuccessful pregnancies and on recent data from patients with autoimmune diseases or with chronic viral infections such as HCV. In particular, we review the role of endocrine factors and IL-2/STAT5 signalling in the impaired expansion of Tregs. Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Published: 2011

24. The most severe forms of type I autoimmune hepatitis are associated with genetically determined levels of TGF-beta1

Author: Natalia Paladino, Esteban Gonzáles Ballerga, Gabriel Costanzo, Miriam Cuarterolo, Lourdes Arruvito, Diana Levi, Leonardo Fainboim, Hugo Tanno, Ana C. Flores, Hugo Fainboim, Teresa Schroder, and Carol Lezama
Subjects: Adult, Male, TYPE I AUTOIMMUNE HEPATITIS, CIENCIAS MÉDICAS Y DE LA SALUD, Adolescent, Genotype, Immunology, Inmunología, Autoimmune hepatitis, Biology, Polymerase Chain Reaction, Polymorphism, Single Nucleotide, INTERLEUKIN 10, Young Adult, TRANSFORMING GROWTH FACTOR-Β1, Transforming Growth Factor beta, medicine, Immunology and Allergy, Humans, Child, Codon, Alleles, SNPS, Aged, Hepatitis, Aged, 80 and over, Age Factors, PAEDIATRIC AND ADULT PATIENTS, Infant, DNA, Hla association, Middle Aged, medicine.disease, Medicina Básica, Hepatitis, Autoimmune, TGF-undefined1, Child, Preschool, IL-10, SINGLE NUCLEOTIDE POLYMORPHISMS, Female, HLA ASSOCIATIONS
Abstract: We previously reported that paediatric (PAH) and adult (AAH) forms of type I autoimmune hepatitis (AH) have different HLA-associations and clinical outcome. In the present study we investigated the role of TGF-β1 genetic polymorphisms in the different outcome of PAH and AAH. We found a significant increase of "high producer" 25GG genotype in PAH and 10CC in AAH. Low inflammation and low fibrosis in AAH was associated with the increase of codon 10CC (high producer) and codon 25CC (low producer) genotypes. The analysis in AAH of the two positions-haplotypes revealed that combined presence of 25GG and 10CC seems to neutralize the 10CC effect which remained in AAH having the 10CC+-25GG- haplotype. Altogether these results may explain, at least partially, the different clinical outcome of AAH and PAH. Fil: Paladino, Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Flores, Ana Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Hugo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina Fil: Schroder, Teresa. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina Fil: Cuarterolo, Miriam. Fundacion Hospital de Pediatria Professor Dr. Juan P. Garrahan; Argentina Fil: Lezama, Carol. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez"; Argentina Fil: Gonzáles Ballerga, Esteban. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Levi, Diana. Gobierno de la Ciudad de Buenos Aires. Hospital de Gastroenterología "Dr. Carlos B. Udaondo"; Argentina Fil: Tanno, Hugo. Universidad Nacional de Rosario. Facultad de Ciencias Médicas; Argentina Fil: Costanzo, Gabriel Gustavo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Published: 2009

25. IL-6 trans-signaling and the frequency of CD4+FOXP3+ cells in women with reproductive failure

Author: Leonardo Fainboim, M. Capucchio, Ariel Billordo, Lourdes Arruvito, and M.E. Prada
Subjects: Adult, Abortion, Habitual, Isoantigens, Regulatory T cell, medicine.medical_treatment, T cell, Immunology, Population, chemical and pharmacologic phenomena, Human leukocyte antigen, Biology, T-Lymphocytes, Regulatory, Immune system, Pregnancy, T-Lymphocyte Subsets, medicine, Cytokine Receptor gp130, Immunology and Allergy, Humans, education, education.field_of_study, Interleukin-6, Immune Sera, Obstetrics and Gynecology, FOXP3, hemic and immune systems, Forkhead Transcription Factors, Mixed lymphocyte reaction, Receptors, Interleukin-6, medicine.anatomical_structure, Cytokine, Reproductive Medicine, CD4 Antigens, Female, Lymphocyte Culture Test, Mixed
Abstract: Pregnancy constitutes a major challenge to the maternal immune system, as it requires tolerance of paternal alloantigen. Maternal rejection of the fetus may develop when T regulatory (Treg) cells fail to control the balance between tolerance and immunity. Increasing evidence supports the role of IL-6 trans-signaling within T cells as a key pathway for blockade of the development of adaptive Treg cells. The present study investigated whether alteration of the components of the IL-6 trans-signaling might be a mechanism associated with modified immune responses in patients experiencing recurrent spontaneous abortion (RSA). In contrast with control women, sera from RSA women induced an enhanced mixed lymphocyte reaction (MLR) against paternal PBMCs, showing increased proliferation and lack of MLR-blocking factor activity. The sera from RSA women inhibited expansion of the FOXP3+ T cell population in TCR-activated PBMCs and showed an imbalance in levels of soluble components of the IL-6 trans-signaling pathway. In comparison with fertile women, those with RSA showed significantly increased levels of soluble IL-6 receptor and IL-6, and decreased levels of soluble gp130, the trans-signaling inhibitor. Finally we found that paternal alloimmunization acts to modulate serum levels of factors involved in the IL-6 trans-signaling pathway and increases the frequency of Treg cells. Consequently, women with reproductive failure show evidence of alteration in the IL-6 trans-signaling pathway which might be associated with abnormal performance of Treg cells in mediating feto-maternal tolerance.
Published: 2008

26. NK cells expressing a progesterone receptor are susceptible to progesterone-induced apoptosis

Author: Marcos Barboza, Leonardo Fainboim, Claudia Lanari, Sebastián Giulianelli, Ana C. Flores, Natalia Paladino, and Lourdes Arruvito
Subjects: Adult, Male, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, Immunology, Inmunología, chemical and pharmacologic phenomena, Apoptosis, Biology, CD16, LIMPHOCYTE SUBSETS, Interleukin 21, Interferon-gamma, Immune system, Internal medicine, Progesterone receptor, medicine, Immunology and Allergy, Humans, Receptor, Progesterone, Cytokine Suppression, SIGNAL TRANSDUCTION, purl.org/becyt/ford/3.1 [https], PROGESTERONE, Bioquímica y Biología Molecular, Interleukin-12, Lymphocyte Subsets, Cell biology, APOPTOSIS, Killer Cells, Natural, Mifepristone, Medicina Básica, Endocrinology, Interleukin 12, Female, purl.org/becyt/ford/3 [https], Signal transduction, Receptors, Progesterone, NK CELLS, Signal Transduction
Abstract: It has been proposed that progesterone (P4) induces the suppression of immune responses, particularly during pregnancy. However, knowledge about the mechanisms involved has remained largely elusive. We demonstrate herein that peripheral blood NK (PBNK) cells express both classical progesterone receptor (PR) isoforms and are specifically affected by the actions of P4 through two apparently independent mechanisms. Progesterone induces caspase-dependent PBNK cell death, which is reversed by two different anti-progestins, ZK 98.299 and RU 486, supporting the involvement of classical PR isoforms. It was suggested that CD56(bright)CD16(-) killer Ig-like receptor (KIR)(-) NK cells might represent precursor cells, which, upon activation, acquire the features of a more mature NK subset expressing KIR receptors. The present study demonstrates that PR expression seems to be restricted to more mature KIR(+) PBNK cells. The expression of PR had a functional counterpart in the suppressive effect of P4 on IL-12-induced IFN-gamma secretion. This cytokine suppression was mainly observed in KIR(+) PBNK cells, without affecting the high secretion of IFN-gamma by CD56(bright) PBNK cells. The lack of PR expression on CD56(bright)KIR(-) PBNK cells provides an additional phenotypic marker to test the idea that they might represent the PBNK precursors selectively recruited into the endometrium where they differentiate to become the uterine NK cells. Additionally, these findings may be relevant to NK cell function in viral immunity, human reproduction, and tumor immunity. Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Giulianelli, Sebastian Jesus. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Flores, Ana Claudia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología, Parasitología e Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Paladino, Natalia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Barboza, Marcos Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Lanari, Claudia Lee Malvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Fainboim, Leonardo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Published: 2008

27. KIR receptors and HLA-C in the maintenance of pregnancy

Author: Derek Middleton, C. Y. Marcos, Leonardo Fainboim, Ana C. Flores, Fionnuala Williams, Natalia Paladino, and Lourdes Arruvito
Subjects: CIENCIAS MÉDICAS Y DE LA SALUD, natural killer cells, Immunology, Inmunología, Human leukocyte antigen, HLA-C Antigens, Biology, Inhibitory postsynaptic potential, recurrent spontaneous abortions, Biochemistry, HLA-C, Gene Frequency, Receptors, KIR, Pregnancy, Genotype, Genetics, medicine, Immunology and Allergy, Humans, Receptors, Immunologic, Receptor, Activating receptors, Inhibitory receptors, General Medicine, medicine.disease, Abortion, Spontaneous, Medicina Básica, KIR immunoglobulin-like receptors, Fertility, Receptors, KIR2DL3, Case-Control Studies, Receptors, KIR2DL2, Receptors, KIR2DL1, Female
Abstract: The present study demonstrated that patients who have recurrent spontaneous abortions (RSA) presented a decreased number of killer immunoglobulin-like inhibitory receptors (KIR), in particular KIR2DL2. The KIR AA genotype was found increased in comparison with controls. Individuals AA will also be homozygous for 2DL3, which in contrast to 2DL2, show a weaker interaction with C1 ligands and therefore a weaker inhibition. The present study might support that in RSA patients, the balance between inhibitory and activating receptors present in natural killer cells is inclined toward an activating state that may contribute to pregnancy loss. Fil: Flores, Ana Claudia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Marcos, C. Y.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina Fil: Paladino, Natalia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Arruvito, Maria Lourdes. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina Fil: Williams, F.. Belfast City Hospital; Irlanda Fil: Middleton, D.. Belfast City Hospital; Irlanda Fil: Fainboim, Leonardo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Published: 2007

28. Increased frequencies of activating natural killer receptors are associated with liver injury in individuals who do not eliminate hepatitis C virus

Author: Leonardo Fainboim, Natalia Paladino, Fionnuala Williams, Ana C. Flores, C. Y. Marcos, Derek Middleton, Lourdes Arruvito, G. Theiler, and Hugo Fainboim
Subjects: hepatitis C virus, Adult, Liver Cirrhosis, Male, Receptors, KIR3DS1, Cirrhosis, CIENCIAS MÉDICAS Y DE LA SALUD, Genotype, Hepatitis C virus, Immunology, Inmunología, Human leukocyte antigen, Hepacivirus, Biology, medicine.disease_cause, Biochemistry, Virus, Gene Frequency, Receptors, KIR, Genetics, medicine, Immunology and Allergy, Humans, Receptors, Immunologic, Receptor, Gene, Aged, Liver injury, natural killer cells, cirrhosis, RNA, Alanine Transaminase, General Medicine, Middle Aged, medicine.disease, Virology, Hepatitis C, HLA, Killer Cells, Natural, Medicina Básica, HLA-B Antigens, RNA, Viral, Female
Abstract: This study was designed to investigate the role of KIR genes in the outcome of HCV infection. In patients who cleared the virus (HCV RNA-) we found a decrease of 2DL2 (p=0.04), and 2DS2 (p=0.014) accompanied by an increase of 2DS5 (p=0.04). Those RNA+ patients with elevated levels of hepatic transaminases (HCV RNA+ elevatedALT) showed an increased frequency of 2DS3 (p=0.018). Additionally, in cirrhotic patients we found an increased frequency of individuals having two copies of 3DS1 and HLA-Bw4 (p=0.016). We conclude that higher NK cytotoxicity might be associated with a worse progression of the HCV infection. Fil: Paladino, Natalia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Flores, Ana Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Marcos, Cintia Yanina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Fainboim, Hugo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina Fil: Theiler, Gerardo Raul. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Williams, F.. Belfast City Hospital; Irlanda Fil: Middleton, D.. Belfast City Hospital; Irlanda Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Published: 2007

29. Sa1248 The Influence of Interleukin-15 on the Expression of CD30 and Ox40 Antigens in Adult Patients With Celiac Disease

Author: Natalia Periolo, Alejandra C. Cherñavsky, Maria Lourdes Arruvito, Hwang Hui Jer, Julio C. Bai, Sonia I. Niveloni, Florencia Vodánovich, and Laura Guillén
Subjects: Hepatology, CD30, Adult patients, Antigen, business.industry, Interleukin 15, Immunology, Gastroenterology, Medicine, Disease, business
Published: 2013

30. Analysis of Suppressor and Non-Suppressor FOXP3+ T Cells in HIV-1-Infected Patients

Author: Julieta Pandolfi, Plácida Baz, Horacio Salomón, Lourdes Arruvito, Juan Sabatté, Jorge Geffner, María Beatriz Lasala, Leonardo Fainboim, and Luis Ariel Billordo
Subjects: CD4-Positive T-Lymphocytes, Human immunodeficiency virus (HIV), lcsh:Medicine, Cell Count, HIV Infections, Stimulation, Adaptive Immunity, medicine.disease_cause, T-Lymphocytes, Regulatory, law.invention, Cohort Studies, law, lcsh:Science, Multidisciplinary, medicine.diagnostic_test, T Cells, FOXP3, Forkhead Transcription Factors, HIV diagnosis and management, hemic and immune systems, Middle Aged, Flow Cytometry, Phenotype, Tissue Donors, Cytokines, Medicine, Infectious diseases, Disease Susceptibility, Research Article, Adult, Immune Cells, Immunology, chemical and pharmacologic phenomena, Viral diseases, Biology, Immune Suppression, Peripheral blood mononuclear cell, Flow cytometry, Young Adult, Diagnostic Medicine, Immune Tolerance, medicine, Humans, Aged, lcsh:R, Immunity, HIV, Lymphocyte Subsets, In vitro, Immune System, HIV-1, Suppressor, Clinical Immunology, lcsh:Q
Abstract: Recently, it was shown that peripheral blood FOXP3+CD4+ T cells are composed of three phenotypic and functionally distinct subpopulations. Two of them having in vitro suppressive effects were characterized as resting Treg cells (rTregs) and activated Treg cells (aTregs). A third subset, identified as FOXP3+ non-Tregs, does not display any suppressor activity and produce high levels of Th1 and Th17 cytokines upon stimulation. In the present study we focus on the characteristics of these three subsets of FOXP3+CD4+ T cells in untreated HIV-1-infected patients. We found that the absolute counts of rTregs, aTregs and FOXP3+ non-Tregs were reduced in HIV-1 patients compared with healthy donors. The relative frequency of rTregs and aTregs was similar in HIV-1 patients and healthy donors, while the frequency of FOXP3+ non-Tregs was significantly higher in HIV-1 patients, reaching a maximum in those patients with the lower values of CD4 counts. Contrasting with the observations made in FOXP3- CD4+ T cells, we did not find a negative correlation between the number of rTregs, aTregs or FOXP3+ non-Tregs and virus load. Studies performed with either whole PBMCs or sorted aTregs and FOXP3+ non-Tregs cells showed that these two populations of FOXP3+ T cells were highly permissive to HIV-1 infection. Upon infection, FOXP3+ non-Tregs markedly down-regulates its capacity to produce Th1 and Th17 cytokines, however, they retain the ability to produce substantial amounts of Th2 cytokines. This suggests that FOXP3+ non-Tregs might contribute to the polarization of CD4+ T cells into a Th2 profile, predictive of a poor outcome of HIV-1-infected patients.
Published: 2012

31. Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children

Author: Leonardo Fainboim, Silvina Raiden, Norma Rivarola, Julieta Pandolfi, Lourdes Arruvito, Mariana Anderson, Jorge Geffner, Fernando Ferrero, Marcela Urtasun, and Florencia Payaslian
Subjects: Male, Pulmonary and Respiratory Medicine, CIENCIAS MÉDICAS Y DE LA SALUD, FOXP3, Syncytial Virus, Medicina Clínica, Respiratory Syncytial Virus Infections, Critical Care and Intensive Care Medicine, Severity of Illness Index, T-Lymphocytes, Regulatory, Virus, Severity of illness, medicine, Bronchiolitis, Viral, Humans, Lymphocyte Count, Respiratory system, Viral immunology, Inflammation, business.industry, Infant, Newborn, Infant, Flow Cytometry, medicine.disease, Virology, Bronchiolitis, Case-Control Studies, Immunology, Female, Medicina Critica y de Emergencia, business, Infants
Abstract: Respiratory syncytial virus (RSV) is the main cause of viral lower respiratory tract illness in infancy and early childhood. Each year, RSV is estimated to cause 34 million cases of lung infection, and the deaths of up to 199 000 children under 5 years of age worldwide. Children are usually infected by RSV during the first year of life, and virtually all by 3 years of age. Although in most cases the infection induces mild illness of the upper airways, 2 to 5% experience a severe bronchiolitis which require hospitalization and respiratory support in an intensive care unit. These patients show later a high susceptibility to develop recurrent wheeze and asthma (1, 2). Our current understanding of the host response to RSV in humans remains rudimentary because most observations have been performed in animal models which do not adequately reflect the course of human infection (3, 4). There is compelling evidence, however, that the host immune response has a prominent role in the pathogenesis of severe RSV infection (3, 4). FOXP3+CD4+ regulatory T cells (Tregs) have emerged as the most important cells able to prevent potentially harmful immune responses (5). Observations made in animal models clearly demonstrated that Tregs play a critical role in controlling lung inflammation in the course of RSV infection (6-8). The presence and function of Tregs during human RSV infection have not been yet analyzed. We here show that severe RSV infection of young children induces the selective depletion of peripheral blood Tregs. Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Pandolfi, Julieta Belen. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Payaslian, Florencia Pía. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Anderson, Mariana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Rivarola Martinez, Norma Gisele. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Ferrero, Fernando Claudio. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina Fil: Urtasun, Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina

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31 results on '"Lourdes Arruvito"'

1. Antibody response against SARS-CoV-2 variants of concern in children infected with pre-Omicron variants: An observational cohort study

2. A poor and delayed anti-SARS-CoV2 IgG response is associated to severe COVID-19 in children

3. Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers

4. Analysis of suppressor and non-suppressor FOXP3+ T cells in HIV-1-infected patients.

5. Infants Younger Than 6 Months Infected With SARS-CoV-2 Show the Highest Respiratory Viral Loads

6. Case Report: Relevance of an Accurate Diagnosis and Monitoring of Infective Dermatitis Associated With Human T-Lymphotropic Virus Type 1 in Childhood

7. A Poor and Delayed Anti-SARS-CoV2 IgG Response is Associated to Severe COVID-19 in Children

8. Fcγ Receptor IIa (FCGR2A) Polymorphism Is Associated With Severe Respiratory Syncytial Virus Disease in Argentinian Infants

9. Upregulation of CD32 in T Cells from Infants with Severe Respiratory Syncytial Virus Disease: A New Costimulatory Pathway?

10. A poor and delayed anti-SARS-CoV2 IgG response is associated to severe COVID-19 in children

11. Blood neutrophils from children with COVID-19 exhibit both inflammatory and anti-inflammatory markers

12. CD32 ligation promotes the activation of CD4+T cells

13. Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease

14. Host response to respiratory syncytial virus infection

15. Purinergic signaling modulates human visceral adipose inflammatory responses: implications in metabolically unhealthy obesity

16. Identification and Clinical Relevance of Naturally Occurring Human CD8+HLA-DR+ Regulatory T Cells

17. Respiratory Syncytial Virus (RSV) Infects CD4+ T Cells: Frequency of Circulating CD4+ RSV+ T Cells as a Marker of Disease Severity in Young Children

18. Regulatory and effector T-cells are differentially modulated by Dexamethasone

19. Expansion of CD4+CD25+and FOXP3+ regulatory T cells during the follicular phase of the menstrual cycle: implications for human reproduction

20. ATP-Induced Inflammation Drives Tissue-Resident Th17 Cells in Metabolically Unhealthy Obesity

21. A physiological role for inducible FOXP3+ TREG cells

22. Cytokines and chronic liver disease

23. Mechanisms involved in the expansion of Tregs during pregnancy: Role of IL-2/STAT5 signalling

24. The most severe forms of type I autoimmune hepatitis are associated with genetically determined levels of TGF-beta1

25. IL-6 trans-signaling and the frequency of CD4+FOXP3+ cells in women with reproductive failure

26. NK cells expressing a progesterone receptor are susceptible to progesterone-induced apoptosis

27. KIR receptors and HLA-C in the maintenance of pregnancy

28. Increased frequencies of activating natural killer receptors are associated with liver injury in individuals who do not eliminate hepatitis C virus

29. Sa1248 The Influence of Interleukin-15 on the Expression of CD30 and Ox40 Antigens in Adult Patients With Celiac Disease

30. Analysis of Suppressor and Non-Suppressor FOXP3+ T Cells in HIV-1-Infected Patients

31. Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children

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31 results on '"Lourdes Arruvito"'

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