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2. Antineutrophil cytoplasmic antibody positivity in IgG4-related disease: A case report and review of the literature

Author

Della Torre Emanuel, Lanzillotta Marco, Campochiaro Corrado, Bozzalla Emanuele, Bozzolo Enrica, Bandiera Alessandro, Bazzigaluppi Elena, Canevari Carla, Modorati Giulio, Stone John H, MANFREDI , ANGELO ANDREA M. A., DOGLIONI , CLAUDIO, DELLA TORRE , EMANUEL, Della Torre, Emanuel, Lanzillotta, Marco, Campochiaro, Corrado, Bozzalla, Emanuele, Bozzolo, Enrica, Bandiera, Alessandro, Bazzigaluppi, Elena, Canevari, Carla, Modorati, Giulio, Stone John, H, Manfredi, ANGELO ANDREA M. A., Doglioni, Claudio, and DELLA TORRE, Emanuel

Subjects
Pathology, medicine.medical_specialty, Biopsy, vasculitis, Subclass, Antibodies, Antineutrophil Cytoplasmic, Diagnosis, Differential, antineutrophil cytoplasmic antibodies, 03 medical and health sciences, rituximab, 0302 clinical medicine, parasitic diseases, medicine, Humans, case report, Clinical Case Report, cardiovascular diseases, 030212 general & internal medicine, IgG4-related disease, skin and connective tissue diseases, Anti-neutrophil cytoplasmic antibody, IgG4, 030203 arthritis & rheumatology, granulomatosis with polyangiitis, integumentary system, medicine.diagnostic_test, business.industry, fungi, General Medicine, Middle Aged, medicine.disease, Immunoglobulin G, Female, Differential diagnosis, Vasculitis, business, Granulomatosis with polyangiitis, Scleritis, Research Article
Abstract

BACKGROUND: IgG4-related disease (IgG4-RD) is a fibroinflammatory condition characterized by serum IgG4 elevation and tissue infiltration of IgG4-positive plasma cells. Substantial overlap between IgG4-RD and antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitides (AAV) exists in terms of organ involvement and histopathological features. A positive ANCA assay is regarded as a highly specific finding in favor of an AAV, and generally influences away from a diagnosis of IgG4-RD. Recent reports, however, have raised the possibility that some patients with IgG4-RD are ANCA positive, thus suggesting reconsideration of the role of ANCA in the diagnostic workup. In the present work, we describe the first case of concomitant biopsy-proven IgG4-RD and granulomatosis with polyangiitis (GPA), demonstrating antiproteinase 3 (PR3) ANCA of the IgG4 subclass in the patient's serum. We also review the literature in order to provide clinicians with tools for interpreting ANCA positivity in IgG4-RD patients. CASE SUMMARY: A 51-year-old woman was referred for left exopthalmos due to lacrimal gland enlargement and increased serum IgG4 concentration. IgG4-RD was suspected and further imaging studies disclosed multiple pulmonary masses in the right lung. Histological analysis of the left lacrimal gland was diagnostic for IgG4-RD, but lung biopsy showed typical features of GPA. ANCA assay was positive for anti-PR3 antibodies. Further immunofluorescence studies demonstrated anti-PR3 antibodies of IgG1 and IgG4 subclass. Treatment with rituximab induced swift remission of both IgG4-RD and GPA manifestations. We identified 9 other reports of patients with IgG4-RD and positive ANCA in the English literature, 5 cases with biopsy-proven IgG4-RD and 4 cases in whom IgG4-RD was diagnosed presumptively. Four patients had also histological evidence of concomitant AAV. CONCLUSION: The present work demonstrates that ANCA positivity in patients with biopsy-proven IgG4-RD should prompt the exclusion of a concomitant vasculitic process; a positive ANCA does not exclude the diagnosis of IgG4-RD; confirmation through immunoenzymatic assays of the ANCA specificity, clinical-pathological correlation, and histopathological evaluation remain crucial steps for the differential diagnosis between AAV and IgG4-RD. ZB 0 Z8 0 ZR 0 ZS 0

Published
2016

5. TRPC6 gene variants and neuropsychiatric lupus

Author

Ramirez GA, Lanzani C, Bozzolo EP, Citterio L, Zagato L, Casamassima N, Canti V, Sabbadini MG, ROVERE QUERINI , PATRIZIA, MANUNTA , PAOLO, MANFREDI , ANGELO ANDREA M. A., Ramirez, Ga, Lanzani, C, Bozzolo, Ep, Citterio, L, Zagato, L, Casamassima, N, Canti, V, Sabbadini, Mg, ROVERE QUERINI, Patrizia, Manunta, Paolo, and Manfredi, ANGELO ANDREA M. A.

Published
2015

8. 7-Tesla Magnetic Resonance Imaging Precisely and Noninvasively Reflects Inflammation and Remodeling of the Skeletal Muscle in a Mouse Model of Antisynthetase Syndrome

Author

Sciorati C, ESPOSITO , ANTONIO, Campana L, Canu T, Monno A, Palmisano A, DE COBELLI , FRANCESCO, DEL MASCHIO , ALESSANDRO, Ascheman Dp, MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, PALMISANO , ANNA, Sciorati, C, Esposito, Antonio, Campana, L, Canu, T, Monno, A, Palmisano, A, DE COBELLI, Francesco, DEL MASCHIO, Alessandro, Ascheman, Dp, Manfredi, ANGELO ANDREA M. A., and ROVERE QUERINI, Patrizia

Subjects
Muscle tissue, Pathology, medicine.medical_specialty, Article Subject, lcsh:Medicine, Inflammation, Antisynthetase syndrome, Biology, General Biochemistry, Genetics and Molecular Biology, medicine, Myocyte, Animals, Muscle, Skeletal, Myositis, Autoantibodies, General Immunology and Microbiology, medicine.diagnostic_test, lcsh:R, Skeletal muscle, Magnetic resonance imaging, General Medicine, medicine.disease, Magnetic Resonance Imaging, Mice, Inbred C57BL, Disease Models, Animal, medicine.anatomical_structure, Diffusion Tensor Imaging, medicine.symptom, Diffusion MRI, Research Article
Abstract

Inflammatory myopathies comprise heterogeneous disorders. Their etiopathogenesis is poorly understood, because of the paucity of informative experimental models and of approaches for the noninvasive study of inflamed tissues. Magnetic resonance imaging (MRI) provides information about the state of the skeletal muscle that reflects various facets of inflammation and remodeling. This technique has been scarcely used in experimental models of inflammatory myopathies. We characterized the performance of MRI in a well-established mouse model of myositis and the antisynthetase syndrome, based on the immunization of wild-type mice with the amino-terminal fragment of histidyl-tRNA synthetase (HisRS). Over an eight-week period following myositis induction, MRI enabled precise identification of pathological events taking place in muscle tissue. Areas of edema and of active inflammation identified by histopathology paralleled muscle modifications detected noninvasively by MRI. Muscles changes were chronologically associated with the establishment of autoimmunity, as reflected by the development of anti-HisRS antibodies in the blood of immunized mice. MR imaging easily appreciated muscle damage and remodeling even if actual disruption of myofiber integrity (as assessed by serum concentrations of creatinine phosphokinase) was limited. Thus, MR imaging represents an informative and noninvasive analytical tool for studyingin vivoimmune-mediated muscle involvement.

Published
2014

11. Leukocyte Hmgb1 controls the regeneration and vascularization of acutely damaged skeletal muscle

Author

Campana L, Santarella F, Rigamonti E, Monno A, Canu T, ESPOSITO, ANTONIO, DEL MASCHIO, ALESSANDRO, BIANCHI, MARCO EMILIO, MANFREDI, ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Campana, L, Santarella, F, Rigamonti, E, Monno, A, Esposito, Antonio, Canu, T, DEL MASCHIO, Alessandro, Bianchi, MARCO EMILIO, Manfredi, ANGELO ANDREA M. A., and ROVERE QUERINI, Patrizia

Published
2013

12. Magnetic resonance imaging at 7T reveals common events in age-related sarcopenia and in the homeostatic response to muscle sterile injury

Author

ESPOSITO , ANTONIO, Campana L, Palmisano A, DE COBELLI , FRANCESCO, Canu T, Santarella F, Colantoni C, Monno A, Vezzoli M, Pezzetti G, MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, DEL MASCHIO , ALESSANDRO, PALMISANO , ANNA, Esposito, Antonio, Campana, L, Palmisano, A, DE COBELLI, Francesco, Canu, T, Santarella, F, Colantoni, C, Monno, A, Vezzoli, M, Pezzetti, G, Manfredi, ANGELO ANDREA M. A., ROVERE QUERINI, Patrizia, and DEL MASCHIO, Alessandro

Subjects
Aging, Sarcopenia, Pathology, Anatomy and Physiology, Mouse, lcsh:Medicine, Diagnostic Radiology, Mice, Myofibrils, Tibialis anterior muscle, Cell Movement, Leukocytes, Homeostasis, lcsh:Science, Musculoskeletal System, Multidisciplinary, medicine.diagnostic_test, Chemistry, Animal Models, Magnetic Resonance Imaging, Diffusion Tensor Imaging, medicine.anatomical_structure, Muscle, Medicine, Female, Radiology, Research Article, medicine.medical_specialty, Immunology, Immunopathology, Cardiotoxins, Model Organisms, Cardiotoxin, Diagnostic Medicine, medicine, Animals, Regeneration, Muscle, Skeletal, Biology, Multiparametric Magnetic Resonance Imaging, Perimysium, lcsh:R, Skeletal muscle, Magnetic resonance imaging, medicine.disease, lcsh:Q, Myofibril, General Pathology
Abstract

"Skeletal muscle remodeling in response to various noxae physiologically includes structural changes and inflammatory events. The possibility to study those phenomena in-vivo has been hampered by the lack of validated imaging tools. In our study, we have relied on multiparametric magnetic resonance imaging for quantitative monitoring of muscle changes in mice experiencing age-related sarcopenia or active regeneration after sterile acute injury of tibialis anterior muscle induced by cardiotoxin (CTX) injection. The extent of myofibrils' necrosis, leukocyte infiltration, and regeneration have been evaluated and compared with parameters from magnetic resonance imaging: T2-mapping (T2 relaxation time; T2-rt), diffusion-tensor imaging (fractional anisotropy, F.A.) and diffusion weighted imaging (apparent diffusion coefficient, ADC). Inflammatory leukocytes within the perimysium and heterogeneous size of fibers characterized aged muscles. They displayed significantly increased T2-rt (P

Published
2013

14. Identification and Predictive Value of Interleukin-6+ Interleukin-10+ and Interleukin-6- Interleukin-10+ Cytokine Patterns in ST-Elevation Acute Myocardial Infarction

Author

Ammirati E, Cannistraci CV, Cristell NA, Vecchio V, Palini AG, Tornvall P, Paganoni AM, Miendlarzewska EA, Sangalli LM, Monello A, Pernow J, BjörnstedtBennermo M, Marenzi G, Hu D, Uren NG, CIANFLONE , DOMENICO, Ravasi T, MANFREDI , ANGELO ANDREA M. A., Maseri A., Ammirati, E, Cannistraci, Cv, Cristell, Na, Vecchio, V, Palini, Ag, Tornvall, P, Paganoni, Am, Miendlarzewska, Ea, Sangalli, Lm, Monello, A, Pernow, J, Björnstedtbennermo, M, Marenzi, G, Hu, D, Uren, Ng, Cianflone, Domenico, Ravasi, T, Manfredi, ANGELO ANDREA M. A., and Maseri, A.

Abstract

"Rationale: At the onset of ST-elevation acute myocardial infarction (STEMI), patients can present with very high circulating interleukin-6 (IL-6(+)) levels or very low-IL-6(-) levels. Objective: We compared these 2 groups of patients to understand whether it is possible to define specific STEMI phenotypes associated with outcome based on the cytokine response. Methods and Results: We compared 109 patients with STEMI in the top IL-6 level (median, 15.6 pg/mL; IL-6(+) STEMI) with 96 in the bottom IL-6 level (median, 1.7 pg/mL; IL-6(-) STEMI) and 103 matched controls extracted from the multiethnic First Acute Myocardial Infarction study. We found minimal clinical differences between IL-6(+) STEMI and IL-6(-) STEMI. We assessed the inflammatory profiles of the 2 STEMI groups and the controls by measuring 18 cytokines in blood samples. We exploited clustering analysis algorithms to infer the functional modules of interacting cytokines. IL-6(+) STEMI patients were characterized by the activation of 2 modules of interacting signals comprising IL-10, IL-8, macrophage inflammatory protein-1α, and C-reactive protein, and monocyte chemoattractant protein-1, macrophage inflammatory protein-1β, and monokine induced by interferon-γ. IL-10 was increased both in IL-6(+) STEMI and IL-6(-) STEMI patients compared with controls. IL-6(+)IL-10(+) STEMI patients had an increased risk of systolic dysfunction at discharge and an increased risk of death at 6 months in comparison with IL-6(-)IL-10(+) STEMI patients. We combined IL-10 and monokine induced by interferon-γ (derived from the 2 identified cytokine modules) with IL-6 in a formula yielding a risk index that outperformed any single cytokine in the prediction of systolic dysfunction and death. Conclusions: We have identified a characteristic circulating inflammatory cytokine pattern in STEMI patients, which is not related to the extent of myocardial damage. The simultaneous elevation of IL-6 and IL-10 levels distinguishes STEMI patients with worse clinical outcomes from other STEMI patients. These observations could have potential implications for risk-oriented patient stratification and immune-modulating therapies."

Published
2012

17. PREGNANCY OUTCOMES IN A COHORT OF AUTOIMMUNE PATIENTS

Author

Rosa S, Franchini S, Sabbadini MG, Canti V, Castiglioni M., MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Rosa, S, Franchini, S, Manfredi, ANGELO ANDREA M. A., Sabbadini, Mg, ROVERE QUERINI, Patrizia, Canti, V, and Castiglioni, M.

Published
2011

20. Redox remodeling: a candidate regulator of HMGB1 function in injured skeletal muscle

Author

Vezzoli M, Castellani P, Campana L, Coma G, Bosurgi L, MANFREDI , ANGELO ANDREA M. A., BIANCHI , MARCO EMILIO, Rubartelli A, ROVERE QUERINI , PATRIZIA, Vezzoli, M, Castellani, P, Campana, L, Coma, G, Bosurgi, L, Manfredi, ANGELO ANDREA M. A., Bianchi, MARCO EMILIO, Rubartelli, A, and ROVERE QUERINI, Patrizia

Published
2010

22. HMGB1 CONTAINING NUCLEOSOMES FROM APOPTOTIC CELLS INDUCE INFLAMMATION AND IMMUNE ACTIVATION VIA TLR2-IMPLICATIONS FOR THE ETIOPATHOGENESIS OF SYSTEMIC LUPUS ERYTHEMATOSUS RID E-7725-2010

Author

Urbonaviciute, V, Fuernrohr, Bg, Meister, S, Munoz, L, Heyder, P, De Marchis, F, Kirschning, C, Wagner, H, Kalden, Jr, Schett, G, Herrmann, M, Voll, Re, BIANCHI, MARCO EMILIO, MANFREDI, ANGELO ANDREA M. A., ROVERE QUERINI, PATRIZIA, Urbonaviciute, V, Fuernrohr, Bg, Meister, S, Munoz, L, Heyder, P, De Marchis, F, Bianchi, MARCO EMILIO, Kirschning, C, Wagner, H, Manfredi, ANGELO ANDREA M. A., Kalden, Jr, Schett, G, ROVERE QUERINI, Patrizia, Herrmann, M, and Voll, Re

Published
2010

25. CYTOKINE DIFFERENTIATION PATTERN IN PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION (STEMI) ASSOCIATED WITH HIGH LEVELS OF CIRCULATING INTELEUKIN (IL)-6

Author

Ammirati E, Cristell N, Cannistraci C, Vecchio V, Paganoni A, Sangalli L, Palini A, Monello A, Banfi M, Uren N, MANFREDI, ANGELO ANDREA M. A., Maseri A., CIANFLONE , DOMENICO, Ammirati, E, Cristell, N, Cannistraci, C, Vecchio, V, Paganoni, A, Sangalli, L, Palini, A, Monello, A, Banfi, M, Uren, N, Manfredi, ANGELO ANDREA M. A., Cianflone, Domenico, and Maseri, A.

Published
2009

27. Immune regulatory neural stem/precursor cells restrain dendritic cell function in secondary lymphoid organs via a BMP-4-dependent mechanism

Author

Zanotti L, Capobianco A, Alfaro Cervello C, Borsellino G, Battistini L, Garcia Verdugo JM, MANFREDI, ANGELO ANDREA M. A., Martino G, Pluchino S., ROVERE QUERINI , PATRIZIA, Zanotti, L, ROVERE QUERINI, Patrizia, Capobianco, A, Alfaro Cervello, C, Borsellino, G, Battistini, L, Garcia Verdugo, Jm, Manfredi, ANGELO ANDREA M. A., Martino, G, and Pluchino, S.

Published
2008

30. HMGB1-Nucleosome complexes from apoptotic cells initiate proinflammatory responses and induce Anti-DsDNA antibodies in mice

Author

Urbonaviciute, V, Furnrohr, Bg, Meister, S, Munoz, L, Heyder, P, Kalden, J, Herrmann, M, Voll, Re, MANFREDI, ANGELO ANDREA M. A., BIANCHI, MARCO EMILIO, ROVERE QUERINI, PATRIZIA, Urbonaviciute, V, Furnrohr, Bg, Meister, S, Munoz, L, Heyder, P, Kalden, J, Manfredi, ANGELO ANDREA M. A., Bianchi, MARCO EMILIO, ROVERE QUERINI, Patrizia, Herrmann, M, and Voll, Re

Published
2008

32. Infusions of HSV-TK engineered donor lymphocytes promote the expansion of host-restricted viral-specific T lymphocytes and protect patients undergoing haploidentical stem cell transplantation from infectious mortality

Author

Provasi E, Stanghellini MTL, Magnani Z, Perna SK, Forcina A, Bernardi M, Peccatori J, Crippa F, Valtolina V, Salomoni M, Turchetto L, Toma S, Traversari C, Colombi S, Stampino CG, MANFREDI, ANGELO ANDREA M. A., BORDIGNON, CLAUDIO, CICERI , FABIO, BONDANZA , ATTILIO, ROVERE QUERINI , PATRIZIA, BONINI , MARIA CHIARA, Provasi, E, Ciceri, Fabio, Stanghellini, Mtl, Bondanza, Attilio, Magnani, Z, Perna, Sk, Forcina, A, Bernardi, M, Peccatori, J, Crippa, F, Valtolina, V, Salomoni, M, Turchetto, L, Toma, S, Traversari, C, Colombi, S, Stampino, Cg, ROVERE QUERINI, Patrizia, Manfredi, ANGELO ANDREA M. A., Bordignon, Claudio, and Bonini, MARIA CHIARA

Published
2007

33. Neuroendocrine modulation induced by selective blockade of TNF-alpha in rheumatoid arthritis

Author

Di Comite G, Marinosci A, Di Matteo P, MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Baldissera E, Aiello P, CORTI , ANGELO, Sabbadini MG, Cutolo M., Di Comite, G, Marinosci, A, Di Matteo, P, Manfredi, ANGELO ANDREA M. A., ROVERE QUERINI, Patrizia, Baldissera, E, Aiello, P, Corti, Angelo, Sabbadini, Mg, and Cutolo, M.

Subjects
Adult, medicine.medical_specialty, Arthritis, General Biochemistry, Genetics and Molecular Biology, Receptors, Tumor Necrosis Factor, Etanercept, Arthritis, Rheumatoid, History and Philosophy of Science, Internal medicine, medicine, Adalimumab, Chromogranins, Humans, Receptor, Aged, biology, business.industry, Tumor Necrosis Factor-alpha, General Neuroscience, Chromogranin A, Antibodies, Monoclonal, Middle Aged, medicine.disease, Neurosecretory Systems, Infliximab, Endocrinology, Rheumatoid arthritis, biology.protein, Tumor necrosis factor alpha, Immunotherapy, business, medicine.drug
Abstract

Tumor necrosis factor-alpha (TNFalpha) is a main actor in the pathogenesis of rheumatoid arthritis (RA), interacting with other molecules in complex mechanisms. The neuroendocrine system is known to be involved and Chromogranin A (CHGA) serum levels are elevated in patients with RA. We evaluated the effect of the selective blockade of TNF-alpha, induced by treatment with anti-TNF-alpha monoclonal antibodies (mAbs), on the serum levels of CHGA and on its correlation with TNF-alpha and TNF-alpha receptors (TNFRs) serum levels. Seven patients with RA have been treated with the anti-TNF-alpha mAb, infliximab. We measured the serum levels of TNF-alpha, its receptors (tumor necrosis factor receptor-I [TNFR-I] and tumor necrosis factor receptor-II [TNFR-II]), and CHGA before and during the treatment. We also measured, as a control, the serum levels of CHGA, TNF-alpha, and soluble TNFRs in 14 patients who were being treated with infliximab, adalimumab, or etanercept and in 20 matching negative controls. The serum levels of TNFR-I and TNFR-II, which are a sensitive marker for the TNF-alpha pathway, correlated with those of CHGA before treatment (Pearson's coefficient, respectively, 0.59 and 0.53). Treatment with anti-TNF-alpha mAb provided a significant clinical response in all patients and the correlation between CHGA and TNFR-I and TNFR-II was no more evident during treatment (respectively, -0.09 and -0.07). TNF-alpha blockade allows a clinical effect in patients with RA and modifies the correlation between CHGA and TNFRs, suggesting that TNF-alpha and CHGA reciprocally interfere in the pathogenesis of RA, through intermediate adaptors, whose identification warrants further studies.

Published
2006

34. HMGB1: an immune odissey

Author

Dumitriu, IE, Baruah, P, Bianchi, ME, MANFREDI , ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, Dumitriu, Ie, Baruah, P, Bianchi, Me, Manfredi, ANGELO ANDREA M. A., and ROVERE QUERINI, Patrizia

Published
2005

35. TNF-alpha coupled to membrane of apoptotic cells favors the cross-priming to melanoma antigens

Author

Zimmermann VS, BONDANZA , ATTILIO, Monno A, ROVERE QUERINI , PATRIZIA, CORTI , ANGELO, MANFREDI , ANGELO ANDREA M. A., Zimmermann, V, Bondanza, Attilio, Monno, A, ROVERE QUERINI, Patrizia, Corti, Angelo, and Manfredi, ANGELO ANDREA M. A.

Abstract

The cross-presentation of Ags derived from apoptotic cell processing contributes to peripheral tolerance. Environmental signals possibly modify this default outcome, favoring cross-priming. In this study, we anchored via a biotin-avidin-biotin bridge soluble TNF-alpha to the membrane of apoptotic melanoma cells and studied in vivo and in vitro the interaction with Ag-presenting phagocytes. TNF-alpha-coated apoptotic melanoma cells injected s.c. had a faster and more efficient access to draining lymph nodes, with cross-priming of melanoma-specific CTLs and delayed outgrowth of melanomas in all treated animals. Twenty. percent of the animals, in the absence of further adjuvant, did not develop the tumor. Immature dendritic cells challenged with TNF-alpha-coated apoptotic melanoma cells secreted proinflammatory cytokines in an autocrine/paracrine fashion, efficiently matured, as assessed functionally and by flow cytometry and cross-presented with enhanced efficiency melanoma Ags to MHC class I- and II-restricted T cells. The results indicate that TNF-alpha targeted to apoptotic membranes, at concentrations that can be safely reached in growing tumors without undue systemic toxicity, influences the outcome of the disposal of dying cells and enhances tumor immunogenicity.

Published
2004

39. The disposal of dying cells in living tissues

Author

MANFREDI , ANGELO ANDREA M. A., Iannacone M, D'Auria F, ROVERE QUERINI , PATRIZIA, Manfredi, ANGELO ANDREA M. A., Iannacone, M, D'Auria, F, and ROVERE QUERINI, Patrizia

Published
2002

40. primary and secondary of the central nervous system

Author

MARTINELLI V, MANFREDI, ANGELO ANDREA M. A., MOIOLA L, SABBADINI MG, COMI , GIANCARLO, VINCENT A, MARTINO G, Martinelli, V, Manfredi, ANGELO ANDREA M. A., Moiola, L, Sabbadini, Mg, and Comi, Giancarlo

Published
2002

44. Anti-beta 2 glycoprotein I antibodies cause inflammation and recruit dendritic cells in platelet clearance

Author

BONDANZA , ATTILIO, MANFREDI , ANGELO ANDREA M. A., Zimmermann VS, Iannacone M, Tincani A, Balestrieri G, Sabbadini MG, ROVERE QUERINI , PATRIZIA, RI Iannacone Matteo/B 3342 2008 Tincani Angela/E 7608 2010, Bondanza, Attilio, Manfredi, ANGELO ANDREA M. A., Zimmermann, V, Iannacone, M, Tincani, A, Balestrieri, G, Sabbadini, Mg, ROVERE QUERINI, Patrizia, and RI Iannacone Matteo/B 3342 2008 Tincani Angela/E 7608, 2010

Subjects
Platelets, business.industry, Antiphospholipid antibodies, Macrophages, Antigen presentation, Inflammation, Hematology, Dendritic cell, Dendritic cells, Proinflammatory cytokine, Tumor necrosis factor-α, Immunology, medicine, Macrophage, Platelet, Platelet activation, medicine.symptom, business, Antigen-presenting cell
Abstract

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.

Published
2001

45. Apoptotic cell-pulsed dendritic cells break tolerance and accelerate lupus in NZB/W F1 mice

Author

BONDANZA , ATTILIO, Sabbadini MG, Zimmermann VS, Dell'Antonio G, Tincani A, Balestrieri G, MANFREDI, ANGELO ANDREA M. A., ROVERE QUERINI , PATRIZIA, RI Tincani Angela/E 7608 2010, Bondanza, Attilio, Sabbadini, Mg, Zimmermann, V, Dell'Antonio, G, Tincani, A, Balestrieri, G, Manfredi, ANGELO ANDREA M. A., ROVERE QUERINI, Patrizia, and RI Tincani Angela/E 7608, 2010

Published
2001

46. Engagement of CD30 shapes the secretion of cytokines by human gamma delta T cells

Author

Biswas P, De Filippi C, Heltai S, Smith C, Ferrarini M., ROVERE QUERINI , PATRIZIA, DAGNA , LORENZO, POLI, GUIDO, MANFREDI , ANGELO ANDREA M. A., Biswas, P, ROVERE QUERINI, Patrizia, De Filippi, C, Heltai, S, Smith, C, Dagna, Lorenzo, Poli, Guido, Manfredi, ANGELO ANDREA M. A., and Ferrarini, M.

Abstract

CD30 is a member of the TNF receptor superfamily, previously shown to be expressed on Hodgkin's lymphoma cells and on normal activated lymphocytes. We here show that CD30 is highly expressed on recently activated human gamma delta T cells. Elevated surface levels of this molecule persisted in long-term cultures of gamma delta cells, without further cell stimulation. CD30 acted as a co-stimulus in gamma delta T cells by potentiating the intracellular Ca2+ fluxes induced by CD3 cross-linking. The engagement of CD30 enhanced the expression of several cytokines induced upon CD3 stimulation such as IL-4 and IFN-gamma but not IL-10. The CC chemokines RANTES and macrophage inflammatory protein-1 beta were constitutively expressed and not affected by stimulation. The inducible expression of the neutrophil chemoattractant IL-8 was enhanced by CD30 co-stimulation, as well as that of the CC chemokines I-309 and MDC, whereas the secretion of the monocyte chemotactic protein-1 was not detected. Triggering of CD30 may therefore modulate the expression of several cytokines released by gamma delta cells; the expression of its physiologic ligand by APC and neutrophils at the site of infection may contribute to determine the outcome of an immune response.

Published
2000

48. Mycobacterium tuberculosis exploits the CD95/CD95 ligand system of gammadelta T cells to cause apoptosis

Author

MANFREDI , ANGELO ANDREA M. A., Heltai S, ROVERE QUERINI , PATRIZIA, Sciorati C, Paolucci C, Gelati G, Rugarli C, Vaiani R, Clementi E, Ferrarini M., Manfredi, ANGELO ANDREA M. A., Heltai, S, ROVERE QUERINI, Patrizia, Sciorati, C, Paolucci, C, Gelati, G, Rugarli, C, Vaiani, R, Clementi, E, and Ferrarini, M.

Subjects
Fas Ligand Protein, Membrane Glycoproteins, T-Lymphocytes, Humans, Apoptosis, Receptors, Antigen, T-Cell, gamma-delta, Mycobacterium tuberculosis, fas Receptor, Cell Line
Abstract

Vgamma9/Vdelta2+ T cells specifically recognize Mycobacterium tuberculosis in vitro and are precociously recruited in early mycobacterial lesions. Even if gammadelta T cells are only fortuitously detected in granulomas or bronchoalveolar lavages of patients with active pulmonary tuberculosis, a role in shaping the mature alphabeta T cell response against M. tuberculosis is substantiated. Here we provide a molecular explanation for this paradox: the engagement of the gammadelta TCR by mycobacterial antigens induced the expression of CD95 ligand (CD95L) by chronically activated CD95+/CD95L- gammadelta T lymphocytes. The receptor was functional, as CD95/CD95L interaction triggered the bystander death of CD95+ cells by apoptosis. Cell death was abolished by CD95-blocking antibodies. The transient accumulation at the site of infection of CD95L+ gammadelta lymphocytes, capable of interacting with CD95+ leukocytes attracted by the response towards the pathogen, may determine the characteristics of the ensuing granulomatous disease.

Published
1998

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