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1. Targeting the Ca2+ Sensor STIM1 by Exosomal Transfer of Ebv-miR-BART13-3p is Associated with Sjögren's Syndrome

Author

Alessia Gallo, Shyh-Ing Jang, Hwei Ling Ong, Paola Perez, Mayank Tandon, Indu Ambudkar, Gabor Illei, and Ilias Alevizos

Subjects
Sjögren's syndrome, microRNA, Exosomes, STIM1, Salivary gland dysfunction, Medicine, Medicine (General), R5-920
Abstract

Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease that is associated with inflammation and dysfunction of salivary and lacrimal glands. The molecular mechanism(s) underlying this exocrinopathy is not known, although the syndrome has been associated with viruses, such as the Epstein Barr Virus (EBV). We report herein that an EBV-specific microRNA (ebv-miR-BART13-3p) is significantly elevated in salivary glands (SGs) of pSS patients and we show that it targets stromal interacting molecule 1 (STIM1), a primary regulator of the store-operated Ca2+ entry (SOCE) pathway that is essential for SG function, leading to loss of SOCE and Ca2+-dependent activation of NFAT. Although EBV typically infects B cells and not salivary epithelial cells, ebv-miR-BART13-3p is present in both cell types in pSS SGs. Importantly, we further demonstrate that ebv-miR-BART13-3p can be transferred from B cells to salivary epithelial cells through exosomes and it recapitulates its functional effects on calcium signaling in a model system.

Published
2016
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2. Autoreactive IgE is prevalent in systemic lupus erythematosus and is associated with increased disease activity and nephritis.

Author

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

Subjects
Medicine, Science
Abstract

The presence of autoantibodies in systemic lupus erythematosus, particularly those of the IgG subclass, have long been associated with disease onset and activity. Here we explored the prevalence of autoreactive IgE in SLE and its relevance to disease in French (n = 79) and United States (US) (n = 117) cohorts with a mean age of 41.5 ± 12.7 and 43.6 ± 15.3 years and disease duration of 13.5 ± 8.5 and 16.6 ± 11.9 years, respectively. Our findings show that approximately 65% of all SLE subjects studied produced IgE antibodies to the seven autoantigens tested. This positivity was increased to almost 83% when only those subjects with active disease were considered. SLE subjects who were positive for anti-dsDNA, -Sm, and -SSB/La -specific IgE showed a highly significant association in the levels of these antibodies with disease activity similar to that of the corresponding IgG's. A strong association of IgE autoantibodies with active nephritis was also found in the combined cohort analysis. A test of the predictive value of autoreactive IgE's and IgGs for disease activity (SLE Disease Activity Index (SLEDAI) ≥ 4) revealed that the best predictors were dsDNA-specific IgE and IgG, and that the age of an SLE subject influenced this predictive model. The finding argue that the overall levels of IgE autoantibodies, independently or in combination with IgG autoantibodies, may serve as indicators of active disease.

Published
2014
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4. Reply: To PMID 23925905

Author

Amit, Golding, Ethan M, Shavach, Sarfaraz, Hasni, and Gabor, Illei

Subjects
Male, Ikaros Transcription Factor, Humans, Lupus Erythematosus, Systemic, Female, Forkhead Transcription Factors, T-Lymphocytes, Regulatory
Published
2014

5. The Percentage of FoxP3+Helios+ Treg Cells Correlates Positively With Disease Activity in Systemic Lupus Erythematosus

Author

Amit, Golding, Sarfaraz, Hasni, Gabor, Illei, and Ethan M, Shevach

Subjects
Adult, Male, Forkhead Transcription Factors, Middle Aged, Methylation, T-Lymphocytes, Regulatory, Article, Ikaros Transcription Factor, Young Adult, Disease Progression, Humans, Lupus Erythematosus, Systemic, Female, Biomarkers
Abstract

To assess the use of Helios in combination with FoxP3 as a superior method for identifying non-cytokine-producing human Treg cells in patients with systemic lupus erythematosus (SLE) and to determine if FoxP3+Helios+ Treg cells are maintained at normal levels in patients with clinically active disease.Peripheral blood mononuclear cells (PBMCs) were purified from the blood of healthy volunteer donors and from 52 consecutive patients with SLE of varying clinical activity (Systemic Lupus Erythematosus Disease Activity Index scores of 0, 2-4, and ≥ 5). PBMCs (either fresh or after 4 hours of stimulation for cytokine production) were then analyzed by flow cytometry for the expression of cell surface markers (CD4, CD25, CD127, and CD45RA) and transcription factors (FoxP3 and Helios), as well as for the production of cytokines (interleukin-2 and interferon-γ).FoxP3+Helios+ Treg cells were found to be non-cytokine producing in both SLE patients and healthy controls. Patients with clinically active SLE had higher percentages of FoxP3+Helios+ Treg cells than did patients with inactive SLE or healthy controls. When corrected for the total CD4 cell count, the absolute numbers of FoxP3+Helios+ Treg cells in patients with moderately-to-highly active SLE were normal.Previous reports of a deficiency in Treg cell number or function in SLE are limited by their use of CD25, either alone or in combination with other markers, to identify human Treg cells. Helios in combination with FoxP3 is a superior method for detecting all non-cytokine-producing Treg cells, irrespective of CD25 or CD45RA expression. Using this method, we showed that FoxP3+Helios+ Treg cell numbers are not reduced in patients with clinically active SLE.

Published
2013

6. List of contributors

Author

Roshini Sarah Abraham, Cristina Albanesi, Ilias Alevizos, Juan Anguita, Gregory M. Anstead, Cynthia Aranow, Howard A. Austin, Subash Babu, Mark C. Ballow, James E. Balow, David R. Barnidge, John W. Belmont, Gabrielle T. Belz, Dina Ben-Yehuda, Claudia Berek, Timothy Beukelman, Thomas Bieber, Johannes W.J. Bijlsma, Jack J.H. Bleesing, Sarah E. Blutt, Barbara Bohle, Elena Borzova, Prosper N. Boyaka, Brockow Knut, Jacinta Bustamante, Frank Buttgereit, Mary Byrne, Virginia L. Calder, Magda Carneiro-Sampaio, Sebastian Carotta, Jean-Laurent Casanova, Lisa A. Cavacini, Edwin S.L. Chan, Javier Chinen, Tanuja Chitnis, Monique Cho, Lisa Christopher-Stine, Andrew P. Cope, David B. Corry, Tricia Cottrell, Antonio Coutinho, Marco Craveiro, Randy Q. Cron, Jennifer Cuellar-Rodriguez, Marinos C. Dalakas, Stephanie C. de Barros, Blythe H. Devlin, Betty Diamond, Angela Dispenzieri, Terry W. Du Clos, Stéphanie Dupuis-Boisson, Todd N. Eagar, Kim D. Edhegard, George S. Eisenbarth, Craig A. Elmets, Doruk Erkan, Mark B. Feinberg, Erol Fikrig, Thomas A. Fleisher, Andrew P. Fontenot, Luis M. Franco, Alexandra F. Freeman, Anthony J. Frew, Thea Friedman, Kohtaro Fujihashi, Massimo Gadina, Stephen J. Galli, H. Bobby Gaspar, Moshe E. Gatt, M. Eric Gershwin, Kamran Ghoreschi, Susan L. Gillespie, Jörg J. Goronzy, Clive E.H. Grattan, Neil S. Greenspan, Eyal Grunebaum, Gabrielle Haeberli, Russell P. Hall, Robert G. Hamilton, Gregory R. Harriman, Sarfaraz A. Hasni, Arthur Helbling, Melanie Hingorani, Steven M. Holland, Petr L. Hruz, Gabor Illei, John B. Imboden, Shai Izraeli, Elaine S. Jaffe, Caroline Jagobi, Sirpa Jalkanen, Pim Jetanalin, Emmanuelle Jouanguy, Carl H. June, Axel Kallies, Stefan H.E. Kaufmann, Arthur Kavanaugh, Sabiha Khan, Farrah Kheradmand, Samia J. Khoury, Gary A. Koretzky, Robert Korngold, Anna Kovalszki, Douglas B. Kuhns, Robert A. Kyle, Ian R. Lanza, Arian Laurence, Susan J. Lee, Michael J. Lenardo, Arnold I. Levinson, Ofer Levy, David B. Lewis, Dorothy E. Lewis, Sue L. Lightman, Michael D. Lockshin, Michael T. Lotze, Amber Luong, Meggan Mackay, Jean-Luc Malo, Jonathan S. Maltzman, Peter J. Mannon, Michael P. Manns, Mary Louise Markert, Elizabeth A. McCarthy, Douglas R. McDonald, Jerry R. McGhee, Peter C. Melby, Dean D. Metcalfe, Martin Metz, Stephen D. Miller, Anna L. Mitchell, Shruti Mittal, Makoto Miyara, Carolyn Mold, David R. Moller, Scott N. Mueller, Ulrich R. Müller, Philip M. Murphy, Pierre Noel, Luigi Notarangelo, Thomas B. Nutman, Stephen L. Nutt, João B. Oliveira, Chris M. Olson, John J. O'Shea, Sung-Yun Pai, Lavannya Pandit, Mary E. Paul, Simon H.S. Pearce, Erik J. Peterson, Capucine Picard, Werner J. Pichler, Stefania Pittaluga, Anne Puel, Andreas Radbruch, Stephen T. Reece, John D. Reveille, Robert R. Rich, Christine Rivat, Bruce W.S. Robinson, John R. Rodgers, Chaim M. Roifman, Antony Rosen, James T. Rosenbaum, Barry T. Rouse, Scott D. Rowley, Shimon Sakaguchi, Marko Salmi, Harry W. Schroeder, Markus J.H. Seibel, Carlo Selmi, William M. Shafer, Prediman K. Shah, Sushma Shankar, Alan R. Shaw, William T. Shearer, Javed Sheikh, Richard Siegel, Anna Simon, Philip L. Simonian, Gideon P. Smith, Justine R. Smith, Andrew L. Snow, David S. Stephens, John H. Stone, Alex Straumann, Helen C. Su, Louise Swainson, Ewa Szymanska-Mroczek, Naomi Taylor, Adrian J. Thrasher, Laura Timares, Raul M. Torres, Gülbŭ Uzel, Jos W.M. van der Meer, Jeroen C.H. van der Hilst, John Varga, Meryl Waldman, Peter Weiser, Peter F. Weller, Cornelia M. Weyand, Theresa L. Whiteside, Fredrick M. Wigley, Robert J. Winchester, Kajsa Wing, Kathryn Wood, Hui Xu, Shen-Ying Zhang, and Valérie S. Zimmermann

Published
2013
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7. The non-muscle Myosin heavy chain 9 gene (MYH9) is not associated with lupus nephritis in African Americans

Author

Barry I, Freedman, Jeffrey C, Edberg, Mary E, Comeau, Mariana, Murea, Donald W, Bowden, Jasmin, Divers, Graciela S, Alarcón, Elizabeth E, Brown, Gerald, McGwin, Jeffrey B, Kopp, Cheryl A, Winkler, George W, Nelson, Gabor, Illei, Michelle, Petri, Rosalind, Ramsey-Goldman, John D, Reveille, Luis M, Vilá, Carl D, Langefeld, and Robert P, Kimberly

Subjects
Adult, Male, Adolescent, Myosin Heavy Chains, Molecular Motor Proteins, Middle Aged, Lupus Nephritis, Polymorphism, Single Nucleotide, Black or African American, Young Adult, Gene Frequency, Haplotypes, Risk Factors, Humans, Female, Genetic Predisposition to Disease, Original Report: Patient-Oriented, Translational Research
Abstract

African Americans (AA) disproportionately develop lupus nephritis (LN) relative to European Americans and familial clustering supports causative genes. Since MYH9 underlies approximately 40% of end-stage renal disease (ESRD) in AA, we tested for genetic association with LN.Seven MYH9 single nucleotide polymorphisms (SNPs) and the E1 risk haplotype were tested for association with LN in three cohorts of AA.A preliminary analysis revealed that the MYH9 E1 risk haplotype was associated with ESRD in 25 cases with presumed systemic lupus erythematosus (SLE)-associated ESRD, compared to 735 non-SLE controls (odds ratio 3.1; p = 0.010 recessive). Replication analyses were performed in 583 AA with SLE in the PROFILE cohort (318 with LN; 265 with SLE but without nephropathy) and 60 AA from the NIH (39 with LN; 21 with SLE but without nephropathy). Analysis of the NIH and larger PROFILE cohorts, as well as a combined analysis, did not support this association.These results suggest that AA with ESRD and coincident SLE who were recruited from dialysis clinics more likely have kidney diseases in the MYH9-associated spectrum of focal segmental glomerulosclerosis. PROFILE and NIH participants, recruited from rheumatology practices, demonstrate that MYH9 does not contribute substantially to the development of LN in AA.

Published
2010

8. List of contributors

Author

Douglas R Adkins, Jane Apperley, Andrew S Artz, Smita Bahtia, Kristin Baird, A John Barrett, Michael R Bishop, Andrew Bodenham, Charles Bolan, Alan K Burnett, Kenneth Carson, Richard Childs, Susan Cleaver, Robin P Corbett, Michele Cottler-Fox, Charles Craddock, H Joachim Deeg, Josu de la Fuente, William B Ershler, Stephen O Evans, Suzanne Fanning, Jürgen Finke, Mary E D Flowers, H Bobby Gaspar, Duncan Gilbert, Eliane Gluckman, Nicola Gökbuget, John M Goldman, John G Gribben, Vikas Gupta, Rupert Handgretinger, Nancy M Hardy, Carolyn Hemsley, Louise Henry, Helen E Heslop, Dieter Hoelzer, Mary Horowitz, Alan Horwich, Edwin Horwitz, Gabor Illei, Armand Keating, Hanna Jean Khoury, Chris Kibbler, Steven Knapper, Samar Kulkarni, Rifca Le Dieu, Zi Yi Lim, Gayle Loader, Chrystal U Louis, Andreas Lundqvist, Judith Marsh, Jayesh Mehta, Simon Meller, Stephan Mielke, Matthew Montgomery, Ghulam J Mufti, Tariq I Mughal, Paolo Muraro, Bijay Nair, John Oram, Steven Pavletic, Gavin D Perkins, Michael Potter, Barry Quinn, Unell Riley, Irene A G Roberts, Vanderson Rocha, James A Russell, Bipin N Savani, Anthony P Schwarer, Bronwen E Shaw, Seema Singhal, Gérard Socié, Shivani Srivastava, John W Sweetenham, Lochie Teague, John Theus, André Tichelli, Jennifer Treleaven, Jaap van Laar, Frits van Rhee, Sumithira Vasu, Paul Veys, Phyllis Warkentin, Alan S Wayne, Daniel Weisdorf, and Robert Wynn

Published
2009
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9. Contributors

Author

Shizuo Akira, Juan Anguita, Gregory M. Anstead, Cynthia Aranow, Howard A. Austin, Subash Babu, James R. Baker, Christopher S. Baliga, Mark Ballow, James E. Balow, Emil J. Bardana, Matthias D. Becker, John W. Belmont, Dina Ben-Yehuda, Claudia Berek, Thomas Bieber, Johannes W.J. Bijlsma, Jack J.H. Bleesing, Sarah E. Blutt, Elena Borzova, Prosper N. Boyaka, Knut Brockow, Ralph C. Budd, Frank Buttgereit, Virginia L. Calder, Fabio Candotti, Sebastian Carotta, Jean-Laurent Casanova, Marilia Cascalho, Edwin S.L. Chan, Javier Chinen, Monique E. Cho, Lisa Christopher-Stine, Helen L. Collins, Andrew P. Cope, Irene Cortese, Bruce N. Cronstein, Adnan Custovic, Marinos C. Dalakas, Blythe H. Devlin, Betty Diamond, Angela Dispenzieri, Joost P.H. Drenth, Terry W. Du Clos, Mark S. Dykewicz, Todd N. Eagar, George S. Eisenbarth, Charles O. Elson, Doruk Erkan, Mark Feinberg, Erol Fikrig, Alain Fischer, Thomas A. Fleisher, Andrew P. Fontenot, Karen A. Fortner, Anthony J. Frew, Thea M. Friedman, Kohtaro Fujihashi, Stephen J. Galli, Moshe E. Gatt, M. Eric Gershwin, Jörg J. Goronzy, Clive E.H. Grattan, Neil S. Greenspan, Beatrix Grubeck-Loebenstein, Gabrielle Haeberli, Russell P. Hall, Robert G. Hamilton, Gregory R. Harriman, Khaled M. Hassan, Arthur Helbling, David B. Hellmann, Vivian Hernandez-Trujillo, Melanie Hingorani, Steven M. Holland, Henry A. Homburger, McDonald Horne, Gabor Illei, John Imboden, Ken J. Ishii, Shai Izraeli, Elaine S. Jaffe, Sirpa Jalkanen, Carl H. June, Barry D. Kahan, Axel Kallies, Stefan H.E. Kaufmann, Arthur F. Kavanaugh, Gary Koretzky, Robert Korngold, Rania D. Kovaiou, Douglas B. Kuhns, Roger Kurlander, Robert A. Kyle, H. Clifford Lane, Arian Laurence, Françoise Le Deist, Susan J. Lee, Steven J. Lemery, Michael J. Lenardo, Arnold I. Levinson, David B. Lewis, Dorothy E. Lewis, Jay Lieberman, Phil Lieberman, Sue L. Lightman, Michael D. Lockshin, Michael T. Lotze, Meggan Mackay, Jonathan S. Maltzman, Michael P. Manns, Markus Y. Mapara, Susana Marinho, M. Louise Markert, Alberto Martini, Seth L. Masters, Evelina Mazzolari, Henry F. McFarland, Jerry R. McGhee, Frank McKenna, Peter C. Melby, Dean D. Metcalfe, Martin Metz, Joann M. Mican, Stephen D. Miller, Carolyn Mold, David R. Moller, Anthony Montanaro, Scott N. Mueller, Ulrich R. Müller, Philip M. Murphy, Pierre Noel, Luigi D. Notarangelo, Thomas B. Nutman, Stephen L. Nutt, João Bosco de Oliveira, Stephen N. Oliver, Chris M. Olson, John O'shea, Mary E. Paul, Erik J. Peterson, Capucine Picard, Werner J. Pichler, Stanley R. Pillemer, Stefania Pittaluga, Jeffrey L. Platt, Paul H. Plotz, Andreas Radbruch, Angelo Ravelli, John D. Reveille, Robert R. Rich, Margaret E. Rick, Kimberly A. Risma, John R. Rodgers, Antony Rosen, James T. Rosenbaum, Marc E. Rothenberg, Barry T. Rouse, Scott Rowley, Martina Rudelius, Shimon Sakaguchi, Marko Salmi, Ulrich E. Schaible, Harry W. Schroeder, Marvin I. Schwarz, Markus J.H. Seibel, Carlo Selmi, William M. Shafer, Prediman K. Shah, Maryam Shahbaz-Samavi, Alan R. Shaw, William T. Shearer, Scott H. Sicherer, Richard Siegel, Ravinder Jit Singh, Justine R. Smith, Phillip D. Smith, Michael C. Sneller, John W. Steinke, David S. Stephens, John H. Stone, Helen C. Su, Cristina M. Tato, Raul M. Torres, Gülbû Uzel, Jeroen C.H. van der Hilst, Jos W.M. van der Meer, John Varga, José A. Villadangos, Su He Wang, Birgit Weinberger, Peter F. Weller, Cornelia M. Weyand, Fredrick M. Wigley, Robert J. Winchester, Kajsa Wing, Louise J. Young, and Li Zuo

Published
2008
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10. Cytokine therapy

Author

Gülbû Uzel, JoAnn M. Mican, John W. Steinke, and Gabor Illei

Subjects
Cytokine Therapy, business.industry, Immunology, Medicine, business
Published
2008
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11. Granulocytic invasion of the central nervous system after hematopoietic stem cell transplantation for systemic lupus erythematosus

Author

Paolo A, Muraro, Nikolay P, Nikolov, John A, Butman, Andrea, Abati, Juan, Gea-Banacloche, Ronald, Gress, Peter, Lipsky, Gabor, Illei, and Steven, Pavletic

Subjects
Adult, Male, Leukocyte Count, Adrenal Cortex Hormones, Central Nervous System Diseases, Neutrophils, Hematopoietic Stem Cell Transplantation, Humans, Lupus Erythematosus, Systemic, Methylprednisolone, Hematopoietic Stem Cell Mobilization, Granulocytes
Abstract

We report on the likely mechanism of an exacerbation of neurological symptoms developed during immune reconstitution after autologous non-myeloablative hematopoietic stem cell transplantation in a 33-year-old man with systemic lupus erythematosus- associated recurrent transverse myelitis. Cerebrospinal fluid examination revealed prominent neutrophilic pleocytosis and no evidence of infection or of reactivation of lupus. Following a course of corticosteroid treatment the exacerbation resolved completely and the patient's neurological function continued to improve, resulting in net gain above pre-treatment for over 1 year follow-up without maintenance immunosuppression. Granulocytic invasion of the central nervous system represents a novel and possibly preventable cause of neurological complications during haematologic reconstitution.

Published
2006

12. Efalizumab down-regulates CD25 expression on FOXP3+ regulatory T cells and exacerbates the autoimmunity in primary Sjogren’s syndrome (96.4)

Author

Dat Tran, Lolita Bebris, Ethan Shevach, and Gabor Illei

Subjects
Immunology, Immunology and Allergy
Abstract

Rationale: FOXP3+ regulatory T cells (Tregs) are central to prevention of autoimmunity. Tregs expressed high level of CD25 and require IL-2 signaling for their function. Since CD25 is up-regulated with activation and LFA-1 is required, we hypothesize that efalizumab treatment would result in down-regulation of CD25 on Tregs and potential exacerbation of autoimmunity. Methods: Subjects with Sjogren’s syndrome were enrolled in a phase II clinical trial for weekly injection of efalizumab (1mg/kg) up to 25 weeks. Peripheral bloods were analyzed for Tregs by flow cytometry. Clinical conditions were measured by objective improvement in salivary and lacrimal flows and minor salivary gland (MSG) inflammation. Results: All three subjects had progressive down-regulation of CD11a and CD18 on Tregs (CD4+FOXP3+), which also correlated with dramatic decrease in CD25. There was no clinical improvement but instead repeat MSG biopsy showed significant increase in inflammation. Two subjects developed anti-dsDNA; one of whom developed multiple autoantibodies and lupus-like syndrome which resolved after efalizumab discontinuation. Conclusions: Efalizumab exacerbates Sjogren’s syndrome and induces significant increase in local inflammation and systemic autoimmunity. Inhibition of LFA-1 interaction on Tregs negatively affected their CD25 without altering their FOXP3 level. This study cautions the potential detrimental effect of efalizumab on Tregs and autoimmunity.

Published
2010
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