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3. FAPi PET/CT for assessment and visualisation of active myositis-related interstitial lung disease: a prospective observational pilot study

Author

Kastrati, Kastriot, Nakuz, Thomas S., Kulterer, Oana C., Geßl, Irina, Simader, Elisabeth, Mrak, Daniel, Bonelli, Michael, Kiener, Hans Peter, Prayer, Florian, Prosch, Helmut, Aletaha, Daniel, Langsteger, Werner, Traub-Weidinger, Tatjana, Blüml, Stephan, Lechner-Radner, Helga, Hacker, Marcus, and Mandl, Peter

Published
2024
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4. Reduced immunogenicity of BNT162b2 booster vaccination in combination with a tetravalent influenza vaccination: results of a prospective cohort study in 838 health workers

Author

Radner, Helga, Sieghart, Daniela, Jorda, Anselm, Fedrizzi, Clemens, Hasenöhrl, Timothy, Zdravkovic, Andrej, Redlberger-Fritz, Monika, Puchammer-Stoeckl, Elisabeth, Anderle, Karolina, Bergmann, Felix, Firbas, Christa, Jordakieva, Galateja, Wagner, Barbara, Haslacher, Helmuth, Perkmann, Thomas, Heinz, Leonhard X., Bonelli, Michael, Crevenna, Richard, Aletaha, Daniel, and Zeitlinger, Markus

Published
2023
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5. Heterologous vector versus homologous mRNA COVID-19 booster vaccination in non-seroconverted immunosuppressed patients: a randomized controlled trial

Author

Mrak, Daniel, Sieghart, Daniela, Simader, Elisabeth, Tobudic, Selma, Radner, Helga, Mandl, Peter, Göschl, Lisa, Koblischke, Maximilian, Hommer, Nikolaus, Wagner, Angelika, Mayer, Margareta, Schubert, Lorenz, Hartl, Lukas, Kozbial, Karin, Hofer, Philipp, Kartnig, Felix, Hummel, Thomas, Kerschbaumer, Andreas, Deimel, Thomas, Puchner, Antonia, Gudipati, Venugopal, Thalhammer, Renate, Munda, Petra, Uyanik-Ünal, Keziban, Zuckermann, Andreas, Novacek, Gottfried, Reiberger, Thomas, Garner-Spitzer, Erika, Reindl-Schwaighofer, Roman, Kain, Renate, Winkler, Stefan, Smolen, Josef S., Stiasny, Karin, Fischer, Gottfried F., Perkmann, Thomas, Haslacher, Helmuth, Zeitlinger, Markus, Wiedermann, Ursula, Aberle, Judith H., Aletaha, Daniel, Heinz, Leonhard X., and Bonelli, Michael

Published
2022
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8. Amino acids fuel fibroblast‐like synoviocyte activation and arthritis by regulating chemokine expression and leukocyte migration

Author

Karonitsch, Thomas, primary, Saferding, Victoria, additional, Kieler, Markus, additional, von Dalwigk, Karolina, additional, Tosevska, Anela, additional, Heller, Gerwin, additional, Dellinger, Mirjam, additional, Niederreiter, Birgit, additional, Kartnig, Felix, additional, Steiner, Carl W., additional, Georgel, Philippe, additional, Kiener, Hans P., additional, Smolen, Josef S., additional, Korb‐Pap, Adelheid, additional, Bonelli, Michael, additional, Aletaha, Daniel, additional, and Blüml, Stephan, additional

Published
2023
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9. The guanine nucleotide exchange factor Rin-like controls Tfh cell differentiation via CD28 signaling

Author

Sandner, Lisa, primary, Alteneder, Marlis, additional, Rica, Ramona, additional, Woller, Barbara, additional, Sala, Eleonora, additional, Frey, Tobias, additional, Tosevska, Anela, additional, Zhu, Ci, additional, Madern, Moritz, additional, Khan, Matarr, additional, Hoffmann, Pol, additional, Schebesta, Alexandra, additional, Taniuchi, Ichiro, additional, Bonelli, Michael, additional, Schmetterer, Klaus, additional, Iannacone, Matteo, additional, Kuka, Mirela, additional, Ellmeier, Wilfried, additional, Sakaguchi, Shinya, additional, Herbst, Ruth, additional, and Boucheron, Nicole, additional

Published
2023
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10. Small extracellular vesicles are released ex vivo from platelets into serum and from residual blood cells into stored plasma

Author

Małys, Małgorzata S., primary, Köller, Maximilian C., additional, Papp, Kristin, additional, Aigner, Christof, additional, Dioso, Daffodil, additional, Mucher, Patrick, additional, Schachner, Helga, additional, Bonelli, Michael, additional, Haslacher, Helmuth, additional, Rees, Andrew J., additional, and Kain, Renate, additional

Published
2023
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11. Asymmetric Action of STAT Transcription Factors Drives Transcriptional Outputs and Cytokine Specificity

Author

Hirahara, Kiyoshi, Onodera, Atsushi, Villarino, Alejandro V., Bonelli, Michael, Sciumè, Giuseppe, Laurence, Arian, Sun, Hong-Wei, Brooks, Stephen R., Vahedi, Golnaz, Shih, Han-Yu, Gutierrez-Cruz, Gustavo, Iwata, Shigeru, Suzuki, Ryo, Mikami, Yohei, Okamoto, Yoshitaka, Nakayama, Toshinori, Holland, Steven M., Hunter, Christopher A., Kanno, Yuka, and O’Shea, John J.

Published
2015
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13. Immunologisch relevante Aspekte der neuen COVID-19-Impfstoffe

Author

Untersmayr, Eva, Förster-Waldl, Elisabeth, Bonelli, Michael, Boztug, Kaan, Brunner, Patrick M., Eiwegger, Thomas, Eller, Kathrin, Göschl, Lisa, Grabmeier-Pfistershammer, Katharina, Hötzenecker, Wolfram, Jordakieva, Galateja, Moschen, Alexander R., Pfaller, Birgit, Pickl, Winfried, Reinisch, Walter, Wiedermann, Ursula, Klimek, Ludger, Bergmann, Karl-Christian, Brehler, Randolf, Novak, Natalija, Merk, Hans F., Rabe, Uta, Schlenter, Wolfgang W., Ring, Johannes, Wehrmann, Wolfgang, Mülleneisen, Norbert K., Wrede, Holger, Fuchs, Thomas, and Jensen-Jarolim, Erika

Subjects
Immunsuppression, Impfwirkung, COVID-19, Immunantwort, COVID-19-Impfung, Immunmodulation, Leitlinie
Published
2021

14. Reduced immunogenicity of BNT162b2 booster vaccination in combination with a tetravalent influenza vaccination: results of a prospective cohort study in 838 health workers

Author

Radner, Helga, primary, Sieghart, Daniela, additional, Jorda, Anselm, additional, Fedrizzi, Clemens, additional, Hasenöhrl, Timothy, additional, Zdravkovic, Andrej, additional, Redlberger-Fritz, Monika, additional, Puchammer-Stoeckl, Elisabeth, additional, Anderle, Karolina, additional, Bergmann, Felix, additional, Firbas, Christa, additional, Jordakieva, Galateja, additional, Wagner, Barbara, additional, Haslacher, Helmuth, additional, Perkmann, Thomas, additional, Heinz, Leonhard X., additional, Bonelli, Michael, additional, Crevenna, Richard, additional, Aletaha, Daniel, additional, and Zeitlinger, Markus, additional

Published
2022
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15. Reactogenicity and immunogenicity of the second COVID-19 vaccination in patients with inborn errors of immunity or mannan-binding lectin deficiency

Author

Göschl, Lisa, primary, Mrak, Daniel, additional, Grabmeier-Pfistershammer, Katharina, additional, Stiasny, Karin, additional, Haslacher, Helmuth, additional, Schneider, Lisa, additional, Deimel, Thomas, additional, Kartnig, Felix, additional, Tobudic, Selma, additional, Aletaha, Daniel, additional, Burgmann, Heinz, additional, Bonelli, Michael, additional, Pickl, Winfried F., additional, Förster-Waldl, Elisabeth, additional, Scheinecker, Clemens, additional, and Vossen, Matthias Gerhard, additional

Published
2022
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18. TNFR2 is critical for TNF-induced rheumatoid arthritis fibroblast-like synoviocyte inflammation

Author

Suto, Takahito, primary, Tosevska, Anela, additional, Dalwigk, Karolina, additional, Kugler, Maximillian, additional, Dellinger, Mirjam, additional, Stanic, Irena, additional, Platzer, Alexander, additional, Niederreiter, Birgit, additional, Sevelda, Florian, additional, Bonelli, Michael, additional, Pap, Thomas, additional, Kiener, Hans, additional, Okamura, Koichi, additional, Chikuda, Hirotaka, additional, Aletaha, Daniel, additional, Heinz, Leonhard X, additional, and Karonitsch, Thomas, additional

Published
2022
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19. Torque Teno Virus quantification for monitoring of immunomodulation with biologic compounds in the treatment of rheumatoid arthritis

Author

Studenic, Paul, primary, Bond, Gregor, additional, Kerschbaumer, Andreas, additional, Bécède, Manuel, additional, Pavelka, Karel, additional, Karateev, Dmitry, additional, Stieger, Jutta, additional, Puchner, Rudolf, additional, Mueller, Ruediger B, additional, Puchhammer-Stöckl, Elisabeth , additional, Durechova, Martina, additional, Loiskandl, Michaela, additional, Perkmann, Thomas , additional, Olejarova, Martina, additional, Luchikhina, Elena, additional, Steiner, Carl-Walter, additional, Bonelli, Michael , additional, Smolen, Josef S, additional, and Aletaha, Daniel, additional

Published
2021
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20. BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis

Author

Roychoudhuri, Rahul, Hirahara, Kiyoshi, Mousavi, Kambiz, Clever, David, Klebanoff, Christopher A., Bonelli, Michael, Sciumè, Giuseppe, Zare, Hossein, Vahedi, Golnaz, Dema, Barbara, Yu, Zhiya, Liu, Hui, Takahashi, Hayato, Rao, Mahadev, Muranski, Pawel, Crompton, Joseph G., Punkosdy, George, Bedognetti, Davide, Wang, Ena, Hoffmann, Victoria, Rivera, Juan, Marincola, Francesco M., Nakamura, Atsushi, Sartorelli, Vittorio, Kanno, Yuka, Gattinoni, Luca, Muto, Akihiko, Igarashi, Kazuhiko, OʼShea, John J., and Restifo, Nicholas P.

Published
2013
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21. Torque Teno Virus quantification for monitoring of immunomodulation with biologic compounds in the treatment of rheumatoid arthritis.

Author

Studenic, Paul, Bond, Gregor, Kerschbaumer, Andreas, Bécède, Manuel, Pavelka, Karel, Karateev, Dmitry, Stieger, Jutta, Puchner, Rudolf, Mueller, Ruediger B, Puchhammer-Stöckl, Elisabeth, Durechova, Martina, Loiskandl, Michaela, Perkmann, Thomas, Olejarova, Martina, Luchikhina, Elena, Steiner, Carl-Walter, Bonelli, Michael, Smolen, Josef S, and Aletaha, Daniel

Subjects
BIOTHERAPY, RESEARCH, RITUXIMAB, VIRUSES, TOCILIZUMAB, IMMUNE system, INFLIXIMAB, ANTIRHEUMATIC agents, TREATMENT effectiveness, RANDOMIZED controlled trials, PRE-tests & post-tests, METHOTREXATE, RHEUMATOID arthritis, STATISTICAL sampling, POLYMERASE chain reaction
Abstract

Objectives RA patients who fail to respond to MTX can receive biologic dMARDs (bDMARDs). The Torque Teno Virus (TTV) is a potential novel candidate for monitoring of immunosuppression. We explore TTV in these patients and its association with clinical response to bDMARDs. Methods The BioBio Study is a multicentre randomized open-label trial, including RA patients with insufficient response to MTX. Patients were randomized to either TNFi (infliximab, INF), anti-IL-6 (tocilizumab, TCZ), CTLA4-Ig (abatacept, ABA) or anti-CD20 (rituximab, RTX) in addition to MTX. PCR was used to quantify TTV in the peripheral blood. Results TTV was measured in 95 patients (INF, n  = 23; TCZ, n  = 22; ABA, n  = 27; RTX; n  = 23). TTV increased by a median of 4.5 × 104 copies/ml [c/ml; interquartile range (IQR) 0–7.5 × 105] after 3 months. TTV levels at month 3 were associated with the Simplified Disease Activity Index (SDAI) (P  = 0.03) and the Clinical Disease Activity Index (CDAI) response (P  = 0.026) at month 6. A TTV cut-off level of 1.2 × 106 c/ml at month 3 had a positive likelihood ratio of 2.7 for prediction of an 85% reduction in SDAI at month 6. Conclusion Our data suggest that TTV levels increase upon TNF, CD20 and costimulation blockade and are associated with the clinical response to bDMARDs in RA patients. Trial registration ClinicalTrials.gov; https://clinicaltrials.gov ; NCT01638715 [ABSTRACT FROM AUTHOR]

Published
2022
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26. HDAC1 fine-tunes Th17 polarization in vivoto restrain tissue damage in fungal infections

Author

Penninger, Philipp, Brezovec, Helena, Tsymala, Irina, Teufl, Magdalena, Phan-Canh, Trinh, Bitencourt, Tamires, Brinkmann, Marie, Glaser, Walter, Ellmeier, Wilfried, Bonelli, Michael, and Kuchler, Karl

Abstract

Histone deacetylases (HDACs) contribute to shaping many aspects of T cell lineage functions in anti-infective surveillance; however, their role in fungus-specific immune responses remains poorly understood. Using a T cell-specific deletion of HDAC1, we uncover its critical role in limiting polarization toward Th17 by restricting expression of the cytokine receptors gp130 and transforming growth factor β receptor 2 (TGF-βRII) in a fungus-specific manner, thus limiting Stat3 and Smad2/3 signaling. Controlled release of interleukin-17A (IL-17A) and granulocyte-macrophage colony-stimulating factor (GM-CSF) is vital to minimize apoptotic processes in renal tubular epithelial cells in vitroand in vivo. Consequently, animals harboring excess Th17-polarized HDCA1-deficient CD4+T cells develop increased kidney pathology upon invasive Candida albicansinfection. Importantly, pharmacological inhibition of class I HDACs similarly increased IL-17A release by both mouse and human CD4+T cells. Collectively, this work shows that HDAC1 controls T cell polarization, thus playing a critical role in the antifungal immune defense and infection outcomes.

Published
2024
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27. MicroRNA-155 Controls T Helper Cell Activation During Viral Infection

Author

Goncalves-Alves, Eliana, primary, Saferding, Victoria, additional, Schliehe, Christopher, additional, Benson, Robert, additional, Kurowska-Stolarska, Mariola, additional, Brunner, Julia Stefanie, additional, Puchner, Antonia, additional, Podesser, Bruno K., additional, Smolen, Josef S., additional, Redlich, Kurt, additional, Bonelli, Michael, additional, Brewer, James, additional, Bergthaler, Andreas, additional, Steiner, Günter, additional, and Blüml, Stephan, additional

Published
2019
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28. Deficiency of Cathelicidin-related Antimicrobial Peptide Promotes Skin Papillomatosis in Mus musculus Papillomavirus 1-infected Mice.

Author

DORFER, Sonja, STRASSER, Katharina, REIPERT, Siegfried, FISCHER, Michael B., SHAFTI-KERAMAT, Saeed, BONELLI, Michael, SCHRÖCKENFUCHS, Georg, BAUER, Wolfgang, KANCZ, Stefanie, MÜLLER, Lena, and HANDISURYA, Alessandra

Subjects
MICE, PAPILLOMAVIRUS diseases, PAPILLOMAVIRUSES, SKIN infections, CELLULAR immunity
Abstract

Cathelicidins have been reported to inhibit human papillomavirus infection in vitro; however, nothing is known about their activity in vivo. In this study, experimental skin infection with Mus musculus papillomavirus 1 resulted in robust development of cutaneous papillomas in cyclosporine A-treated C57BL/6J mice deficient for the murine cathelicidin-related antimicrobial peptide (CRAMP), in contrast to wild-type controls. Analysis of the underlying mechanisms revealed moderate disruption of virion integrity and lack of interference with viral entry and intracellular trafficking by a synthetic CRAMP peptide. Differences in the immune response to Mus musculus papillomavirus 1 infection were observed between CRAMP-deficient and wildtype mice. These included a stronger reduction in CD4+ and CD8+ T-cell numbers in infected skin, and lack of Mus musculus papillomavirus 1-specific neutralizing antibodies in response to cyclosporine A in the absence of endogenous CRAMP. CRAMP has modest direct antipapillomaviral effects in vitro, but exerts protective functions against Mus musculus papillomavirus 1 skin infection and disease development in vivo, primarily by modulation of cellular and humoral immunity. [ABSTRACT FROM AUTHOR]

Published
2021
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29. CCR6 controls autoimmune but not innate immunity-driven experimental arthritis

Author

Bonelli, Michael, primary, Puchner, Antonia, additional, Göschl, Lisa, additional, Hayer, Silvia, additional, Niederreiter, Birgit, additional, Steiner, Guenter, additional, Tillmann, Katharina, additional, Plasenzotti, Roberto, additional, Podesser, Bruno, additional, Georgel, Philippe, additional, Smolen, Josef, additional, Scheinecker, Clemens, additional, and Blüml, Stephan, additional

Published
2018
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31. Mus musculuspapillomavirus 1 is a key driver of skin cancer development upon immunosuppression

Author

Dorfer, Sonja, Strasser, Katharina, Schröckenfuchs, Georg, Bonelli, Michael, Bauer, Wolfgang, Kittler, Harald, Cataisson, Christophe, Fischer, Michael B., Lichtenberger, Beate M., and Handisurya, Alessandra

Abstract

Epidemiological and experimental data implicate cutaneous human papillomavirus infection as co‐factor in the development of cutaneous squamous cell carcinomas (cSCCs), particularly in immunocompromised organ transplant recipients (OTRs). Herein, we established and characterized a skin cancer model, in which Mus musculuspapillomavirus 1 (MmuPV1) infection caused cSCCs in cyclosporine A (CsA)‐treated mice, even in the absence of UV light. Development of cSCCs and their precursors were observed in 70% of MmuPV1‐infected, CsA‐treated mice on back as well as on tail skin. Immunosuppression by systemic CsA, but not UV‐B irradiation, was a prerequisite, as immunocompetent or UV‐B–irradiated mice did not develop skin malignancies after infection. In the virus‐driven cSCCs the MmuPV1‐E6/E7 oncogenes were abundantly expressed, and transcriptional activity and productive infection demonstrated. MmuPV1 infection induced the expression of phosphorylated H2AX, but not degradation of proapoptotic BAK in the cSCCs. Transfer of primary cells, established from a MmuPV1‐induced cSCC from back skin, into athymic nude mice gave rise to secondary cSCCs, which lacked viral DNA, demonstrating that maintenance of the malignant phenotype was virus independent. This papillomavirus‐induced skin cancer model opens future investigations into viral involvement, pathogenesis, and cancer surveillance, aiming at understanding and controlling the high incidence of skin cancer in OTRs. This murine model demonstrates the synergy of Mus musculuspapillomavirus 1 skin infection and systemic immunosuppression in the development of cutaneous squamous cell carcinomas, even in the absence of UV‐B light.

Published
2021
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32. Transcriptional and epigenetic networks that drive helper T cell identities

Author

Shih, Han-Yu, Sciumè, Giuseppe, Poholek, Amanda C, Vahedi, Golnaz, Hirahara, Kiyoshi, Villarino, Alejandro V, Bonelli, Michael, Bosselut, Remy, Kanno, Yuka, Muljo, Stefan A, and O’Shea, John J.

Subjects
Immunomodulation, Immunity, Cellular, T-Lymphocyte Subsets, Animals, Humans, Cell Differentiation, Cell Lineage, Gene Regulatory Networks, T-Lymphocytes, Helper-Inducer, Transcriptome, Article, Immunity, Innate, Epigenesis, Genetic
Abstract

The discovery of the specification of CD4(+) helper T cells to discrete effector 'lineages' represented a watershed event in conceptualizing mechanisms of host defense and immunoregulation. However, our appreciation for the actual complexity of helper T-cell subsets continues unabated. Just as the Sami language of Scandinavia has 1000 different words for reindeer, immunologists recognize the range of fates available for a CD4(+) T cell is numerous and may be underestimated. Added to the crowded scene for helper T-cell subsets is the continuously growing family of innate lymphoid cells (ILCs), endowed with common effector responses and the previously defined 'master regulators' for CD4(+) helper T-cell subsets are also shared by ILC subsets. Within the context of this extraordinary complexity are concomitant advances in the understanding of transcriptomes and epigenomes. So what do terms like 'lineage commitment' and helper T-cell 'specification' mean in the early 21st century? How do we put all of this together in a coherent conceptual framework? It would be arrogant to assume that we have a sophisticated enough understanding to seriously answer these questions. Instead, we review the current status of the flexibility of helper T-cell responses in relation to their genetic regulatory networks and epigenetic landscapes. Recent data have provided major surprises as to what master regulators can or cannot do, how they interact with other transcription factors and impact global genome-wide changes, and how all these factors come together to influence helper cell function.

Published
2014

33. Signal transducer and activator of transcription 5 (STAT5) paralog dose governs T cell effector and regulatory functions

Author

Villarino, Alejandro, primary, Laurence, Arian, additional, Robinson, Gertraud W, additional, Bonelli, Michael, additional, Dema, Barbara, additional, Afzali, Behdad, additional, Shih, Han-Yu, additional, Sun, Hong-Wei, additional, Brooks, Stephen R, additional, Hennighausen, Lothar, additional, Kanno, Yuka, additional, and O'Shea, John J, additional

Published
2016
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35. Phosphatase and tensin homolog (PTEN) in antigen-presenting cells controls Th17-mediated autoimmune arthritis

Author

Blüml, Stephan, primary, Sahin, Emine, additional, Saferding, Victoria, additional, Goncalves-Alves, Eliana, additional, Hainzl, Eva, additional, Niederreiter, Birgit, additional, Hladik, Anastasia, additional, Lohmeyer, Tobias, additional, Brunner, Julia S., additional, Bonelli, Michael, additional, Koenders, Marije I., additional, van den Berg, Wim B., additional, Superti-Furga, Giulio, additional, Smolen, Josef S., additional, Schabbauer, Gernot, additional, and Redlich, Kurt, additional

Published
2015
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36. EZH2 is crucial for both differentiation of regulatory T cells and T effector cell expansion

Author

Yang, Xiang-Ping, primary, Jiang, Kan, additional, Hirahara, Kiyoshi, additional, Vahedi, Golnaz, additional, Afzali, Behdad, additional, Sciume, Giuseppe, additional, Bonelli, Michael, additional, Sun, Hong-Wei, additional, Jankovic, Dragana, additional, Kanno, Yuka, additional, Sartorelli, Vittorio, additional, O’Shea, John J., additional, and Laurence, Arian, additional

Published
2015
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38. Autoreactive IgE Is Prevalent in Systemic Lupus Erythematosus and Is Associated with Increased Disease Activity and Nephritis

Author

Dema, Barbara, primary, Pellefigues, Christophe, additional, Hasni, Sarfaraz, additional, Gault, Nathalie, additional, Jiang, Chao, additional, Ricks, Tiffany K., additional, Bonelli, Michael M., additional, Scheffel, Jörg, additional, Sacré, Karim, additional, Jablonski, Mathieu, additional, Gobert, Delphine, additional, Papo, Thomas, additional, Daugas, Eric, additional, Illei, Gabor, additional, Charles, Nicolas, additional, and Rivera, Juan, additional

Published
2014
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39. CD4+CD25-Foxp3+ T cells: a marker for lupus nephritis?

Author

Bonelli, Michael, primary, Göschl, Lisa, additional, Blüml, Stephan, additional, Karonitsch, Thomas, additional, Steiner, Carl-Walter, additional, Steiner, Günter, additional, Smolen, Josef S, additional, and Scheinecker, Clemens, additional

Published
2014
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40. BACH2 represses effector programmes to stabilize Treg-mediated immune homeostasis - a new target in tumor immunotherapy?

Author

Roychoudhuri, Rahul, primary, Hirahara, Kiyoshi, additional, Mousavi, Kambiz, additional, Clever, David, additional, Bonelli, Michael, additional, Klebanoff, Christopher, additional, Sartorelli, Vittorio, additional, Kanno, Yuka, additional, Gattinoni, Luca, additional, Wang, Ena, additional, Liu, Hui, additional, Marincola, Franco, additional, Kazuhiko, Igarashi, additional, O’Shea, John, additional, and Restifo, Nicholas P, additional

Published
2013
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42. Strain-Specific Properties and T Cells Regulate the Susceptibility to Papilloma Induction by Mus musculus Papillomavirus 1.

Author

Handisurya, Alessandra, Day, Patricia M., Thompson, Cynthia D., Bonelli, Michael, Lowy, Douglas R., and Schiller, John T.

Subjects
T cells, PAPILLOMA, MOUSE diseases, HAPLOTYPES
Abstract

The immunocytes that regulate papillomavirus infection and lesion development in humans and animals remain largely undefined. We found that immunocompetent mice with varying H-2 haplotypes displayed asymptomatic skin infection that produced L1 when challenged with 6×1010 MusPV1 virions, the recently identified domestic mouse papillomavirus (also designated “MmuPV1”), but were uniformly resistant to MusPV1-induced papillomatosis. Broad immunosuppression with cyclosporin A resulted in variable induction of papillomas after experimental infection with a similar dose, from robust in Cr:ORL SENCAR to none in C57BL/6 mice, with lesional outgrowth correlating with early viral gene expression and partly with reported strain-specific susceptibility to chemical carcinogens, but not with H-2 haplotype. Challenge with 1×1012 virions in the absence of immunosuppression induced small transient papillomas in Cr:ORL SENCAR but not in C57BL/6 mice. Antibody-induced depletion of CD3+ T cells permitted efficient virus replication and papilloma formation in both strains, providing experimental proof for the crucial role of T cells in controlling papillomavirus infection and associated disease. In Cr:ORL SENCAR mice, immunodepletion of either CD4+ or CD8+ T cells was sufficient for efficient infection and papillomatosis, although deletion of one subset did not inhibit the recruitment of the other subset to the infected epithelium. Thus, the functional cooperation of CD4+ and CD8+ T cells is required to protect this strain. In contrast, C57BL/6 mice required depletion of both CD4+ and CD8+ T cells for infection and papillomatosis, and separate CD4 knock-out and CD8 knock-out C57BL/6 were also resistant. Thus, in C57BL/6 mice, either CD4+ or CD8+ T cell-independent mechanisms exist that can protect this particular strain from MusPV1-associated disease. These findings may help to explain the diversity of pathological outcomes in immunocompetent humans after infection with a specific human papillomavirus genotype. [ABSTRACT FROM AUTHOR]

Published
2014
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44. BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis.

Author

Roychoudhuri, Rahul, Hirahara, Kiyoshi, Mousavi, Kambiz, Clever, David, Klebanoff, Christopher A., Bonelli, Michael, Sciumè, Giuseppe, Zare, Hossein, Vahedi, Golnaz, Dema, Barbara, Yu, Zhiya, Liu, Hui, Takahashi, Hayato, Rao, Mahadev, Muranski, Pawel, Crompton, Joseph G., Punkosdy, George, Bedognetti, Davide, Wang, Ena, and Hoffmann, Victoria

Subjects
AUTOIMMUNE diseases, HOMEOSTASIS, ASTHMA, CROHN'S disease, TRANSCRIPTION factors, T cells, GENETIC polymorphisms, MULTIPLE sclerosis
Abstract

Through their functional diversification, distinct lineages of CD4+ T cells can act to either drive or constrain immune-mediated pathology. Transcription factors are critical in the generation of cellular diversity, and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage commitment. Genetic polymorphisms within a single locus encoding the transcription factor BACH2 are associated with numerous autoimmune and allergic diseases including asthma, Crohn's disease, coeliac disease, vitiligo, multiple sclerosis and type 1 diabetes. Although these associations point to a shared mechanism underlying susceptibility to diverse immune-mediated diseases, a function for BACH2 in the maintenance of immune homeostasis has not been established. Here, by studying mice in which the Bach2 gene is disrupted, we define BACH2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programs of multiple effector lineages in CD4+ T cells. BACH2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg-cell-dependent. Assessment of the genome-wide function of BACH2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, BACH2 constrained full effector differentiation within TH1, TH2 and TH17 cell lineages. These findings identify BACH2 as a key regulator of CD4+ T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. [ABSTRACT FROM AUTHOR]

Published
2013
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45. CD4+CD25-Foxp3+T cells: a marker for lupus nephritis?

Author

Bonelli, Michael, Göschl, Lisa, Blüml, Stephan, Karonitsch, Thomas, Steiner, Carl-Walter, Steiner, Günter, Smolen, Josef, and Scheinecker, Clemens

Abstract

Systemic lupus erythematosus (SLE) is a heterogenous autoimmune disease, which can affect different organs. Increased proportions of CD4+CD25-Foxp3+T cells have been described in SLE patients. The exact role of this cell population in SLE patients still remains unclear. We therefore analyzed this T cell subset in a large cohort of SLE patients with different organ manifestations. Phenotypic analyses, proportions and absolute cell numbers of CD4+CD25-Foxp3+T cells were determined by flow cytometry (FACS) in healthy controls (HC) (n = 36) and SLE patients (n = 61) with different organ manifestations. CD4+CD25-Foxp3+T cells were correlated with clinical data, the immunosuppressive therapy and different disease activity indices. In patients with active glomerulonephritis, CD4+CD25-Foxp3+T cells were analyzed in urine sediment samples. Time course analyses of CD4+CD25-Foxp3+T cells were performed in patients with active disease activity before and after treatment with cyclophosphamide and prednisone. CD4+CD25-Foxp3+T cells were significantly increased in active SLE patients and the majority expressed Helios. Detailed analysis of this patient cohort revealed increased proportions of CD4+CD25-Foxp3+T cells in SLE patients with renal involvement. CD4+CD25-Foxp3+T cells were also detected in urine sediment samples of patients with active glomerulonephritis and correlated with the extent of proteinuria. CD4+CD25-Foxp3+T cells resemble regulatory rather than activated T cells. Comparative analysis of CD4+CD25-Foxp3+T cells in SLE patients revealed a significant association of this newly described cell population with active nephritis. Therefore CD4+CD25-Foxp3+T cells might serve as an important tool to recognize and monitor SLE patients with renal involvement.

Published
2014
Full Text
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46. Gestione Efficiente di Eventi Complessi su Piattaforma IoT ThingWorx

Author

Bonelli, Michael, thesis supervisor: Bellavista, Paolo, Bonelli, Michael, and thesis supervisor: Bellavista, Paolo

Abstract

Nella prima parte di questa tesi viene introdotto il concetto di Internet of Things. Vengono discussi gli elementi costituitivi fondamentali di tale tecnologia, le differenti architetture proposte nel corso degli anni e le sfide che devono ancora essere affrontate per vedere realizzato l’IoT. Questa prima parte si conclude inoltre con due esempi di applicazione dell’IoT. Questi due esempi, Smart City e Smart Healthcare, hanno l’obbiettivo di evidenziare quali sono i vantaggi ed i servizi che possono essere offerti all’utente finale una volta applicato l’IoT. Nel secondo capitolo invece, vengono presentate le funzionalità della piattaforma IoT ThingWorx, la quale mette a disposizione un ambiente di sviluppo per applicazioni IoT con l’obbiettivo di ridurre i tempi e quindi anche i costi di sviluppo delle stesse. Questa piattaforma cerca di ridurre al minimo la necessità di scrivere codice, utilizzando un sistema di sviluppo di tipo “Drag and Drop”. ThingWorx mette anche a disposizione degli SDK per facilitare la programmazione dei device, gestendo soprattutto la parte di comunicazione nodo – piattaforma. Questo argomento viene trattato ampiamente nella parte finale di questo capitolo dopo aver visto quali sono i concetti fondamentali di modellazione e rappresentazione dei dati sui quali si basa la piattaforma. Nel terzo e ultimo capitolo di questa tesi viene presentato innanzitutto il tutorial Android di ThingWorx. Svolgere e successivamente estendere il tutorial ha evidenziato alcune limitazioni del modello iniziale e questo ci ha portato a progettare e sviluppare il componente Aggregated & Complex Event Manager per la gestione di eventi complessi e che permette di sgravare parzialmente la piattaforma da tale compito. La tesi si conclude evidenziando, tramite dei test, alcune differenze fra la situazione iniziale nella quale il componente non viene utilizzato e la situazione finale, nella quale invece viene usato.

47. Gestione Efficiente di Eventi Complessi su Piattaforma IoT ThingWorx

Author

Bonelli, Michael, thesis supervisor: Bellavista, Paolo, Bonelli, Michael, and thesis supervisor: Bellavista, Paolo

Abstract

Nella prima parte di questa tesi viene introdotto il concetto di Internet of Things. Vengono discussi gli elementi costituitivi fondamentali di tale tecnologia, le differenti architetture proposte nel corso degli anni e le sfide che devono ancora essere affrontate per vedere realizzato l’IoT. Questa prima parte si conclude inoltre con due esempi di applicazione dell’IoT. Questi due esempi, Smart City e Smart Healthcare, hanno l’obbiettivo di evidenziare quali sono i vantaggi ed i servizi che possono essere offerti all’utente finale una volta applicato l’IoT. Nel secondo capitolo invece, vengono presentate le funzionalità della piattaforma IoT ThingWorx, la quale mette a disposizione un ambiente di sviluppo per applicazioni IoT con l’obbiettivo di ridurre i tempi e quindi anche i costi di sviluppo delle stesse. Questa piattaforma cerca di ridurre al minimo la necessità di scrivere codice, utilizzando un sistema di sviluppo di tipo “Drag and Drop”. ThingWorx mette anche a disposizione degli SDK per facilitare la programmazione dei device, gestendo soprattutto la parte di comunicazione nodo – piattaforma. Questo argomento viene trattato ampiamente nella parte finale di questo capitolo dopo aver visto quali sono i concetti fondamentali di modellazione e rappresentazione dei dati sui quali si basa la piattaforma. Nel terzo e ultimo capitolo di questa tesi viene presentato innanzitutto il tutorial Android di ThingWorx. Svolgere e successivamente estendere il tutorial ha evidenziato alcune limitazioni del modello iniziale e questo ci ha portato a progettare e sviluppare il componente Aggregated & Complex Event Manager per la gestione di eventi complessi e che permette di sgravare parzialmente la piattaforma da tale compito. La tesi si conclude evidenziando, tramite dei test, alcune differenze fra la situazione iniziale nella quale il componente non viene utilizzato e la situazione finale, nella quale invece viene usato.

48. CD4⁺CD25⁻Foxp3⁺ T cells: a marker for lupus nephritis?

Author

Bonelli M, Göschl L, Blüml S, Karonitsch T, Steiner CW, Steiner G, Smolen JS, and Scheinecker C

Subjects
Adult, Female, Flow Cytometry, Forkhead Transcription Factors immunology, Humans, Immunophenotyping, Male, Middle Aged, Phenotype, Biomarkers blood, CD4-Positive T-Lymphocytes immunology, Lupus Nephritis immunology, T-Lymphocyte Subsets immunology
Abstract

Introduction: Systemic lupus erythematosus (SLE) is a heterogenous autoimmune disease, which can affect different organs. Increased proportions of CD4⁺CD25-Foxp3⁺ T cells have been described in SLE patients. The exact role of this cell population in SLE patients still remains unclear. We therefore analyzed this T cell subset in a large cohort of SLE patients with different organ manifestations., Methods: Phenotypic analyses, proportions and absolute cell numbers of CD4⁺CD25-Foxp3⁺ T cells were determined by flow cytometry (FACS) in healthy controls (HC) (n = 36) and SLE patients (n = 61) with different organ manifestations. CD4⁺CD25⁻Foxp3⁺ T cells were correlated with clinical data, the immunosuppressive therapy and different disease activity indices. In patients with active glomerulonephritis, CD4⁺CD25⁻Foxp3⁺ T cells were analyzed in urine sediment samples. Time course analyses of CD4⁺CD25⁻Foxp3⁺ T cells were performed in patients with active disease activity before and after treatment with cyclophosphamide and prednisone., Results: CD4⁺CD25⁻Foxp3⁺ T cells were significantly increased in active SLE patients and the majority expressed Helios. Detailed analysis of this patient cohort revealed increased proportions of CD4⁺CD25⁻Foxp3⁺ T cells in SLE patients with renal involvement. CD4⁺CD25⁻Foxp3⁺ T cells were also detected in urine sediment samples of patients with active glomerulonephritis and correlated with the extent of proteinuria., Conclusion: CD4⁺CD25⁻Foxp3⁺ T cells resemble regulatory rather than activated T cells. Comparative analysis of CD4⁺CD25⁻Foxp3⁺ T cells in SLE patients revealed a significant association of this newly described cell population with active nephritis. Therefore CD4⁺CD25⁻Foxp3⁺ T cells might serve as an important tool to recognize and monitor SLE patients with renal involvement.

Published
2014
Full Text
View/download PDF

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