Leading the way to a cure

For Researchers

Target Identification in Lupus Grants

 Application information will be available in the Winter of 2015

If you have any questions or require any additional information regarding the application process, please contact the ALR’s Research Administration department at 1-212-218-2840, 1-800-867-1743 or by e-mail at research.admin@lupusresearch.org.

Clinical Trials Request for Posting

Corporations, CRO’s and Investigators if you have clinical trials that you would like the ALR to post information on please click here for more information.

Below you will find links to some Clinical Trials that are looking For Researchers, Patients and to share data.

These trials are in no way affiliated with the ALR and are for informational Purposes only.

Efficacy and Safety of Atacicept in Systemic Lupus Erythematosus

  • Atacicept is a targeted B-Cell immunomodulator which inhibits APRIL and BLyS effect as well as auto-antibody inhibition. A Phase IIb, Multi-Center, Randomized, Double-Blind, Placebo-Controlled, Multidose, 24-Week Study to Evaluate the Efficacy and Safety of Atacicept in Subjects With Systemic Lupus Erythematosus (SLE).

Embrace (Efficacy of Belimumab in Lupus Subjects of Black Race)

  • A phase 3/4, Multi-Center, Randomized, Double-Blind, Placebo-Controlled, 52 Week Study to Evaluate the Efficacy and Safety of Belimumab in Adult Subjects of Black Race with Systemic Lupus Erythematosus.

Bliss- SC Belimumab International SLE Study – Subcutaneous

  • A Phase 3, Multi-Center, Randomized, Double-Blind, Placebo-Controlled, 52-Week Study to Evaluate the Efficacy and Safety of Belimumab (HGS1006) Administered Subcutaneously to Subjects with Systemic Lupus Erythematosis (SLE).

Belimumab (Benlysta) Pregnancy Registry - Prospective Cohort Study of Pregnancy Outcomes following Belimumab Exposure

  • The Belimumab Pregnancy Registry is a global, observational cohort study. It will collect prospective pregnancy outcome data on a voluntary basis in women with systemic lupus erythematosus (SLE) who have received belimumab (Benlysta). Infant outcomes from babies born to mothers in this Registry will also be evaluated. Registry data will add to the current clinical experience with belimumab and complement reproductive data from animal toxicology studies. This Registry is sponsored by GlaxoSmithKline (GSK) and managed by Pharmaceutical Product Development (PPD), Inc

Bliss – LN Belimumab International Lupus Nephritis Study

  • A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Belimumab plus Standard of Care Induction and Maintenance Therapy for Active Lupus Nephritis.

PLUTO – (Pediatric Lupus Trial Of belimumab)

  • A Multi-Center, Randomized Parallel Group, Placebo-Controlled Double-Blind trial to Evaluate the Safety, Efficacy, and Pharmacokinetics of Belimumab, A Human Monoclonal Anti-BLyS Antibody, Plus Standard Therapy in Pediatric Patients with SLE.

SABLE SLE Registry

  • A 5-Year Prospective Observational Registry to Assess Adverse Events of Interest and Effectiveness in Adults with Active, Autoantibody-Positive SLE Treated with or without BENLYSTA (belimumab) (SABLE).

BASE (Belimumab Assessment of Safety in SLE)

  • A Randomized, Double-Blind, Placebo-Controlled 52 Week Study to Assess Adverse Events of Special Interest in Adults with Active, Autoantibody-Positive Systemic Lupus Erythematosus Receiving Belimumab.

Mary K. (Peggy) Crow, M.D. (Chair)

Dr. Crow is Physician-in-Chief and Chair of the Department of Medicine at Hospital for Special Surgery and is Chief of the Division of Rheumatology at HSS and NewYork-Presbyterian/Weill Cornell Medical Center. She is also Director of the Autoimmunity and Inflammation Research Program and Co-Director of the Mary Kirkland Center for Lupus Research at HSS. Dr. Crow holds the Benjamin M. Rosen Chair in Immunology and Inflammation Research at HSS and is the Joseph P. Routh Professor of Rheumatic Diseases in Medicine at Weill Cornell Medical College.

Dr. Crow leads 66 full-time physicians, including 30 adult and 3 pediatric rheumatologists, who provide outstanding care to patients across the full spectrum of autoimmune and inflammatory rheumatic diseases and deliver perioperative medical care to patients undergoing surgical procedures at HSS. Dr. Crow has established disease-specific Centers of Excellence focused on innovative initiatives in clinical and translational research, patient and professional education, and quality of care.

Dr. Crow’s academic and research career has focused on unraveling the cellular and molecular mechanisms that underlie the systemic autoimmune diseases, with a particular focus on systemic lupus erythematosus and rheumatoid arthritis. She has identified interferon-alpha, an immune system protein typically expressed in the setting of virus infection, as the key pathogenic mediator in lupus. Her laboratory continues to study the molecular pathways that are associated with the clinical manifestations of lupus and the mechanisms that result in disease flares.

In addition to her leadership roles at HSS and NYPH/WCMC, Dr. Crow has served as President of the American College of Rheumatology and as President of the Henry Kunkel Society. She has been honored as an “Arthritis Hero” of the Arthritis Foundation, and in 2010 she received the Margaret D. Smith Lifetime Achievement Award of the Arthritis Foundation, New York Chapter.

Anthony J. Coyle, Ph.D.

Anthony “Tony” Coyle is Vice President and Chief Scientific Officer of the Centers for Therapeutic Innovation (CTI). CTI was established in August 2010 as a new model to drive innovation in BioTherapeutics R & D. Tony is responsible for the CTI sites, which currently include CTI – New York City, CTI- Boston and CTI-California. Tony is supported by his leadership team, which will include the site heads of each CTI, his operations team, project management, clinical and Precision Medicine heads.

Tony brings an extensive knowledge of the full development process to Pfizer. As a former Vice President and Global Head of Respiratory, Inflammation, and Autoimmunity Research at Medimmune Biologics, a Division of AstraZeneca, Tony has succeeded in advancing a biologic portfolio from discovery to Phase Two in the areas of Lupus, Asthma and COPD.

Prior to Medimmune, Tony was Director of Research and Biology at Millennium Pharmaceuticals, where he led a group responsible for the identification of novel target genes as well as for late stage lead optimization and delivery of both small molecule and biologic development candidates.

Tony has been Associate Professor in the Department of Pathology and Experimental Therapeutics at McMaster University in Ontario since 1992, and has authored more than 180 manuscripts. He holds a B.Sc. Honours and a Ph.D. from Kings College, University of London.

Saeed Fatenejad M.D.

Richard Furie, M.D.

Dr. Richard Furie, Chief of the Division of Rheumatology and Allergy-Clinical Immunology at the North Shore LIJ Health System, is a rheumatologist whose activities for the last several decades have focused on patient care, physician education, and clinical research in the area of anti-rheumatic drug development. He directs The Program in Novel Therapeutics, the Health System’s clinical research program in musculoskeletal disease. He also directs the Hospital’s SLE and Autoimmune Disease Treatment Center, which has become internationally recognized for its role in the development of new therapies for SLE. Regarded as one the senior rheumatologists in the New York metropolitan area, he has been on the Boards of Directors of the local chapters of the Arthritis Foundation and the Lupus Alliance of America and is a member of the Medical-Scientific Advisory Council of the Lupus Foundation of America as well as its Lupus News editorial board. He also is on the Medical and Scientific Advisory Board of the SLE Foundation as well as the Alliance for Lupus Research Scientific Advisory Board. Dr. Furie has served on many committees of the American College of Rheumatology, and has recently been appointed to the College’s Board of Directors.

Kenneth Kalunian, M.D.

Dr. Kalunian is a Professor of Medicine in the Division of Rheumatology, Allergy and Immunology at the University of California, San Diego (UCSD). Dr. Kalunian is the Associate Director of UCSD’s Center for Innovative Therapy and directs clinical investigation in lupus for the Center including the conduct of industry-sponsored, NIH and foundation-directed, and investigator-initiated clinical trials. Dr. Kalunian is particularly interested in the development of novel therapeutic interventions for lupus including biological agents and small molecules; these include not only the testing of novel approaches to therapy but also the design and validation of outcome instruments for these clinical studies. Other research focuses include the study of epidemiological characteristics of lupus with particular interest in phenotypic subsets and translational and outcome studies that focus on these subsets. Prior to joining the faculty at UCSD in 2003, Dr. Kalunian was on the faculty at UCLA, where he trained in translational and basic science of lupus with particular interest in the pathogenesis of the disease. Dr. Kalunian also started UCLA’s clinical trial program in lupus. Dr. Kalunian is currently the Chair of the Lupus Foundation of America’s Collective Data Analysis Initiative, which is involved in better understanding outcomes of lupus patients in clinical trials using data from multiple industry-sponsored clinical trials. Dr. Kalunian is on the Medical Scientific Advisory Board of the Lupus Foundation of America, is a member of the Lupus Clinical Trials Consortium, is a founding member of the Systemic Lupus International Collaborating Clinics, is a member of the Lupus Nephritis Trials Network and is a member of the UCSD Clinical Translational Research Institute. Dr. Kalunian is a past president of the Southern California Rheumatology Society. Dr. Kalunian is a fellow of the American College of Rheumatology and received his Bachelor’s Degree in Biochemistry from Occidental College, his Medical Degree from St. Louis University, and completed his Internal Medicine and Rheumatology training at UCLA.

Mike McCune, M.D., Ph.D.

Research in the McCune Lab has focused on the definition of pathogenic mechanisms of viral diseases, particularly HIV disease. This focus has spanned a range of fields, from understanding critical structural determinants of infectivity, to devising a small animal model (the SCID-hu Thy/Liv mouse) to study HIV pathogenesis and to prioritize antiretroviral compounds against HIV, to studying mechanisms of T cell depletion and repletion in vivo. Throughout this body of work, he has engaged in hypothesis-driven, patient-oriented research that has involved collaborative teams of basic scientists, translational researchers, and clinicians. Most recently, he has devoted all of his attention to understanding the correlates of protective immunity against HIV, with the specific intent to work with others to eradicate HIV. This change of focus has now been materialized at UCSF by the creation of the Division of Experimental Medicine, of which Dr. McCune is the Chief. From 2005-2008, he served as the PI and Director of the Clinical and Translational Science Institute at UCSF, an organization whose mission is to enhance and to facilitate the process by which better therapies can be brought from the lab bench to the community more quickly. In this capacity, he also served as the Senior Associate Dean of Clinical and Translational Research in the Schools of Dentistry, Medicine, Nursing, and Pharmacy at UCSF.

In the Division of Experimental Medicine, he has established a multidisciplinary, collaborative environment for the analysis of the human immunology of chronic infectious diseases of medical importance, including those caused by HIV, TB, malaria, and helminthic worms. The underlying hypothesis of the Division is that each of these agents has established patterns of interaction with the host which, in most cases, do not lead to overt disease; that these patterns are likely to embrace protective immune responses with mechanistic overlaps; and that elucidation of such common patterns of successful host-pathogen interaction may inform the development of interventions (e.g., vaccines and medicines) to successfully fight HIV.

Jane Salmon, M.D.

Dr. Jane Salmon is Professor of Medicine and Professor of Obstetrics and Gynecology at Weill Cornell Medical College and the Collette Kean Research Professor at Hospital for Special Surgery.

Dr. Salmon graduated magna cum laude from New York University and earned a medical degree in 1978 from the College of Physicians and Surgeons of Columbia University, where she was the first woman enrolled in their Medical Scientist Training Program. She completed training in internal medicine at The New York Hospital and in rheumatology at Hospital for Special Surgery, and has been an HSS faculty member since 1983. Dr. Salmon has served on the Board of Directors of the American College of Rheumatology and as Councilor of the Clinical Immunology Society. She has served on the NIH Advisory Boards for the North American Rheumatoid Arthritis Consortium and the Lupus Multiplex Registry and was co-editor of Arthritis and Rheumatism. At Hospital for Special Surgery, she is a co-Director of the Mary Kirkland Center for Lupus Research, Director of the SLE APS Center of Excellence, Director of the FOCIS Center of Excellence, and Director of the Lupus Registry and Repository.

Dr. Salmon’s research has focused on elucidating mechanisms of tissue injury in lupus and other autoimmune diseases. Her basic and clinical studies have expanded our understanding of pregnancy loss and organ damage in SLE and the determinants of disease outcome in lupus patients with nephritis, pregnancy, and cardiovascular disease.

George Tsokos, M.D.

Dr. Tsokos received his Medical Degree and a Doctorate in Sciences from the University of Athens. He trained in Internal Medicine at the University of Athens and Georgetown University/VA Medical Center in Washington DC and completed Immunology and Rheumatology Fellowships at the National Institutes of Health. Between 1987 and 2007 he was a member of the Uniformed Services/Walter Reed community where served in various positions including Vice Chair for Research in the Department of Medicine and Chief of the Department of Cell Injury. In 2007 he joined the Beth Israel Medical Center as Chief of Rheumatology and Harvard Medical School as Professor of Medicine.

He has served various leadership positions including President of the Clinical Immunology Society and as member or chair of multiple federal study sections and editorial boards of scientific journals. He has served (or serves) as Consulting Editor of the Journal of Clinical Investigation, Editor of Autoimmunity, Academic Editor of PLOS One and Editor-in-Chief of Clinical Immunology. He has been elected to the Association of American Physicians, Fellow of the American Association for the Advancement of Sciences and Master of the American College of Physicians.

Dr. Tsokos’ research focuses on the cellular and molecular pathogenesis of systemic lupus erythematosus (SLE). His laboratory has opened and led the field of molecular abnormalities on immune cells in patients with SLE. He has identified several molecular abnormalities, including aberrant expression of CD3 zeta chain, cAMP response element modulator, calcium-calmodulin kinase IV and protein phosphatase 2A and demonstrated that when their expression is corrected in cells obtained from patients with SLE with either gene transfer or small molecule drugs the effector cell function returns to normal levels. More recently he has constructed a series of novel mice to demonstrate in vivo the importance of the molecules expressed aberrantly in SLE T cells in the expression of autoimmunity and organ damage.

Dr. Tsokos has trained over 100 colleagues many of whom hold senior leadership positions and run independent laboratories and has published more than 450 articles. His research is funded by NIH and DoD grants.

2014 Alliance for Lupus Research Scientific Calendar

View Our special reports on the ACR and other Meetings

February 1, 2015 2014 Target Identification in Lupus (TIL) Grants Activated  
February 28, 2015 LuCIN Applications Due  
March 19, 2015 Lupus Insight Prize Application Due  
June 24, 2015 Lupus Insight Prize Ceremony  
December 2015 Scientific Advisory Board Meeting  

Scientific Meetings

Jan 25-31, 2014 Winter Rheumatology Symposium – Snowmass, Colorado
March 7-9, 2014 Third Inaugural Meeting of the Lupus Academy – Berlin, Germany
March 26-30, 2014 9th International Congress on Autoimmunity – Nice, France
March 31- April 4, 2014 16th Asia Pacific League of Associations for Rheumatology – Cebu City, Philippines
May 2-6, 2014 The American Association of Immunologists – IMMUNOLOGY 2014 – Pittsburg, Pennsylvania
June 11-14, 2014 EULAR 2014 Paris, France
June 25-28, 2014 Federation of Clinical Immunology Societies 2014 – Chicago, Illinois
July 1-4, 2014 Frontiers in Immunology Research International Conference – Florence, Italy
October 12-16, 2014 International Conference on Nervous System Autoimmunity – Goa, India
November 14-19, 2014 ACR/ARHP 77TH Annual Scientific Meeting – Boston, Massachusetts
March 12-14, 2015 CORA 2015: Controversies in Rheumatology & Autoimmunity – Sorrento, Italy - Happens every two years
August 21-26, 2016 International Congress of Immunology – Melbourne, Australia - Happens every three years

Special Reports

View Highlights from the ALR's 2013 American College of Rheumatology Annual Scientific Meeting

View highlights from the ALR's 2011 American College of Rheumatology Annual Scientific Meeting

View highlights from the ALR's 2010 American College of Rheumatology Annual Scientific Meeting

View the Lupus Congress 2010 Special Report

Understanding the MoA of Low Dose IL-2 as a Potential Therapy for SLE

Interleukin 2 (IL-2) is one of the immune system’s signaling molecules.  Therapy with low dose IL-2 has proven efficacious and safe in two diseases similar to lupus: chronic graft-versus-host disease (GVHD) and hepatitis C virus  (HCV) vasculitis.  The therapy achieves both expansion of regulatory T cells (Tregs) and diminished levels of pro-inflammatory chemicals (cytokines) in the blood of treated persons, and has been found to be safe. Tregs are able to suppress aberrant pathological immune responses and so guide the immune system not to attack healthy tissue.  The mechanism of action of low dose IL-2 has not yet been fully elucidated, while it is known that this mechanism of action is related to the presence on Tregs of a specific receptor (the high affinity IL-2 receptor). The presence of this receptor permits the preferential activation of this subset of regulatory T cells (Tregs)  without activation of T helper cells.  Will therapy with low dose Il-2, or a related approach, prove to be effective in lupus patients? 

What this means for people with lupus:  Dr. Fathman’s current project seeks to elucidate the mechanism of action underlying the use of low dose IL-2 as a therapy, and to determine whether signaling cascades similar to those described can be activated in T regs derived from lupus patients.  In addition, he will search for complementary therapies that could, along with low dose IL-2, lead to the restoration of Treg function in lupus patients. 

Therapeutic targeting of FcgRIIb on B cells in SLE

B cells function in ways vital to the immune system, allowing humans to ward off and better cope with often-hostile bacteria, viruses, and other foreign matter.  However, B cells also play a central role in the development of lupus, as they possess the capacity to attack not only foreign invaders but also to mistakenly work against patients’ own cells and tissues.  It might be therapeutic to inhibit those B cells that promote disease; but this would be beneficial only if this is accomplished in a way that does not undermine the protective capacity of B cells. What does the human body itself do to regulate B cells? Without depleting the supply of B cells, the human body regulates B cells by inhibiting them. In the normal, healthy functioning of the immune system, immune complexes (IC) down-regulate ongoing immune responses by co-engaging cognate BCR with FcgRIIb. (The B cell receptor [BCR] is a specialized receptor protein present on the surface of B cells. The Fc region receptor II-b [FcgRIIb] is a surface receptor protein that modulates B cell activity.)  Certain specific monoclonal antibodies (mAbs) – proteins that scientists have produced in a laboratory -- function in ways similar to the way a healthy immune system regulates B cells, and, so, might be developed as a lupus therapy. Dr. Stohl has bred lupus-prone mice possessing the human FcgRIIb gene.  In the current project, he will use mAbs in a mouse lupus model to assess the effects of BCR/FcgRIIb co-engagement on B cell activation. In addition, he will investigate how such BCR/FcgRIIb co-engagement affects the clinical, immunological, and pathological features of a mouse lupus model.

What this means for people with lupus:  Having a single agent that effects high-affinity co-engagement of the BCR complex and FcgRIIb can potently inhibit the activation and functioning of the B cells associated with lupus.  Will a mAb prevent the development of lupus in a mouse model of the disease?  Will it effectively and safely treat established disease in mice? Dr. Stohl hopes his research will lay a foundation for a novel lupus therapy.

The cyclic GAMP Pathway in SLE

Researchers have recently identified a previously unknown pathway involved in the production of type 1 interferons; and type 1 interferons – powerful stimulators of the immune system – play a role in the development of lupus.  This new finding demonstrated the importance of an enzyme called cGAMP synthase  (cGAS).  It is now known that cGAS, in turn, encourages the production of cGAMP (cyclic-GMP-AMP) and cGAMP, in turn, binds to and activates a protein named STING leading to the production of type 1 interferons. Previously, Dr. Elkon has detected activation of the cGAS pathway in some (not all) patients with lupus. Using mass spectrometry and additional approaches, he will now explore what an activated cGAS pathway means for a lupus patient. For example, are these people with early onset or late onset disease? Do they have more or less severe disease? Do they have a specific subtype of the disease? He will also investigate the specific cell types in which cGAS is activated and will explore what stimulates such activation. His research holds the potential to elucidate pathogenic mechanisms relevant to the illness. Dr. Elkon’s current research has a second aim, as well: Laboratory experiments suggest that three drugs currently used to treat malaria might be re-engineered so they can be used to inhibit the cGAS pathway. He will, initially, study the modified drugs in mouse models of lupus.  These drugs are already known to have an excellent safety profile in the setting of lupus.

What this means for people with lupus: Dr. Elkon’s research seeks to, first, identify a novel biomarker for lupus, and explore what that biomarker might tell us about the disease and whether it can be implicated in some (but not all) people with the illness. And, second, his research will investigate, through mouse studies of modified drugs, whether these drugs might be safely tested in people with lupus.   

The contribution of epigenetics to SLE phenotype and outcome

The essential genetic structure – in other words, the DNA sequence -- of a cell may remain unchanged while, at the same time, multiple factors, including environmental factors, may lead to long-term changes in the expression of a cell’s genes. Epigenetics is the area of biology that studies such processes and activities. Accumulating evidence points to the role of epigenetic changes in autoimmune diseases, including lupus: The link between a person’s susceptibility to developing lupus and environmental factors may reside (in part at least) in epigenetic activity. In addition, the study of epigenetics may provide clues as to why specific treatments are most effective in subsets of lupus patients.  Previously, Dr. Criswell had completed preliminary studies demonstrating that people with severe lupus symptoms and people with mild lupus symptoms exhibit different patterns of epigenetic changes. Dr. Criswell’s current research project aims (1) to use data from an ongoing longitudinal study and to apply a novel methodology to determine which specific cell subpopulation(s) are responsible for epigenetic differences between lupus patients with severe versus mild disease. She will simultaneously explore whether epigenetic changes influence response to treatment. In addition, she will (2) further characterize epigenetic changes associated with lupus by exploring correlations with levels of gene expression:  She will study quantitative gene expression patterns.

What this means for people with lupus:  Dr. Criswell’s overall goal for this project is to define the mechanisms through which differences in epigenetic alterations influence the pattern and severity of symptoms in individual lupus patients and certain types of lupus patients.  Further, it is known that several medications currently approved to treat other illnesses successfully target epigenetic mechanisms; and Dr. Criswell would like to determine if some of these medications might provide benefit to lupus patients. (And, if so, the fact that these medicines are known to be safe and have been approved by the Food and Drug Administration (FDA) as therapies for other illnesses should hasten their availability as therapies for lupus.)

Targeting IL-10 producing B cells in SLE

Interleukin-10 (IL-10) is a cytokine that, in multiple ways, helps to regulate the immune system.  IL-10 appears to play a role in the pathogenesis of lupus: (1) elevated levels of IL-10 in the blood of lupus patients correlates with elevated disease activity and promotes B-cell hyperactivity and autoantibody production (2) early results of a novel anti-IL-10 monoclonal antibody treatment in lupus patients appear promising, and (3) specific genetic variants of the IL-10 gene are associated with increased risk for developing lupus and other autoimmune diseases.   Assessing IL-10 gene cluster variants, Tsao and colleagues recently identified the crucial lupus-risk allele. In addition, they demonstrated that this allele (1) has genome-wide significance,  (2) exhibits a dose-dependent relationship to elevated levels of IL-10 in the blood circulation of lupus patients and healthy controls, and (3) preferentially binds to a transcription factor (Elk-1). In people possessing the implicated genetic variant, activation of Elk-1 augments IL-10 production. An unexpected finding of this research was that Elk-1 activation constitutes a general feature of lupus and active lupus disease is associated with increased proportions of B cells expressing both  IL-10 and activated Elk-1, which promotes production of IL-10 and autoantibodies.  In healthy people, IL-10 producing B cells  (B10 cells) function to regulate the immune system; in lupus, they function abnormally.   Tsao and colleagues propose to study the major defective mechanism(s) responsible for the overproduction of IL-10 and of the defective regulatory function of B10 cells, they will then be able to target specific mechanisms --  leading to a reduction of disease activity.

What this means for people with lupus:  The long-term goal is to develop a new therapeutic approach to lupus that might in the near future be tested in a mouse model of the disease.

Sex and microbiota influence on immunoregulation and disease in BWF1 mice

Male sex steroids (androgens) appear to protect men from developing lupus, and even men with a genetic susceptibility to the disease appear to be protected though this mechanism. Recent studies have shown that androgens affect the bacteria that naturally live in the digestive tract and that, in turn, these bacteria (the gut microbiota) influence the activities of androgens.  For example, recent research suggests that the microbiota and androgens may collaborate to protect male mice from autoimmune diseases, such as type 1 diabetes.  Using a mouse lupus model, Dr Kosiewicz’s preliminary studies have found that the microbiota and related factors differ between females and males, and transfer of male microbiota to female mice protects the females from disease and increases mouse length of life. It may be (but this has not been proven) that substances (metabolites) produced by the microbiota of males protects males through activation of certain immune system components. Perhaps such substances (or the entities that produce these substances) would be useful in treating lupus in females.   In the current study, Dr. Kosiewicz will (1) use a mouse model of lupus to identify certain products of gut microbiota influenced by androgens; (2) explore the role of various products of male-imprinted gut microbiota in preventing lupus; and (3) determine the role of specific immune cells (intestinal dendritic cells) in these protective processes.

What this means for people with lupus:  Dr. Kosiewicz will test the hypothesis that androgen-modified male microbiota produce substances that protect against lupus by acting through specific immune cells.  She hopes the current research will lead to the development of novel lupus therapies that make use of the products of microbiota. (She would also like to discover similar therapies that target other autoimmune diseases).

Role of Tim-1 in kidneys during lupus

Lupus nephritis, the most common manifestation of the disease, is associated with increased risk of end-stage renal disease and death. Dr. Xiao’s research focuses on a molecule that might play an important role in generating kidney damage in lupus patients.  Various teams of scientists have given this single molecule several different names: one is kidney injury molecule (KIM-1) and another is T-cell immunoglobulin and mucin domain 1 (TIM-1).   Elevated levels of KIM-1/TIM-1 are not found in the kidneys of healthy people. However, high levels of KIM-1/TIM-1 are present in the kidneys of people with lupus nephritis (as well as in the kidneys of people with kidney injury and of people with kidney diseases unrelated to lupus).  The role of KIM-1/TIM-1 in lupus nephritis and other kidney disorders has not been well studied.   During successive stages of research, Dr Xiao has generated several varieties of mutant mice relevant to the investigation of the role of Tim-1 in lupus nephritis: some of these mice lack certain functions associated with Tim-1, other sets of mice he has generated over express Tim-1 in kidney cells, and still other sets of mice exhibit a lack of Tim-1 in certain contexts. Other teams of scientists have published additional studies relevant to Dr Xiao’s investigations.  

What this means for people with lupus:  Knowledge about the possible role of KIM-1/TIM-1 in lupus nephritis has accumulated. Plus, a number of mutant mouse models and other tools relevant to the study of the possible role of KIM-1/TIM-1 are now available. Dr Xiao hopes to determine conclusively if Tim-1 affects lupus nephritis in animal models of the disease – and, if it does, to arrive at a scientific understanding of how this occurs. Such understanding would likely provide insights into the disease mechanism of lupus in people. The long-term hope is that this research will lead to the development of novel therapeutic strategies for treating lupus nephritis in lupus patients.

Role for SHP2 as a therapeutic target for systemic lupus erythematosus

SHP2 is an enzyme, a protein that helps regulate certain activities in the human body. Among other functions, SHP2 helps modulate the body’s response to stress by inducing inflammation.  Previously, Dr. Kontaridis demonstrated that there is elevated SHP2 activity in the cells of people with lupus, a finding that suggests SHP2 is involved in the disease mechanism underlying lupus. Using a newly created, potent, and specific inhibitor for SHP2, Dr. Kontaridis then conducted experiments in a mouse model of lupus. Just six weeks of treatment with this inhibitor improved disease symptoms and prevented kidney and spleen damage. Importantly, the inhibitor caused no harmful side effects.  She then isolated specific cells of the immune system directly affected by SHP2 activity and showed that SHP2 caused increased growth in a specific subset of these cells, causing the increased inflammatory response that ultimately leads to the organ and tissue damage associated with lupus.

What this means for people with lupus:  Taken together, Dr. Kontaridis’experiments suggest that inhibiting SHP2 activity might prove beneficial for people with lupus – although this has not yet been proven clinically.  If in the future the approach does prove beneficial for patients, then this research will have identified a new, potent, and targeted lupus therapy.

Regulation of T Follicular Helper Cells in SLE by E3 Ubiquitin Ligase Cbl-­‐b

Among the multiple arms of the immune system involved in lupus, the activation of certain specific cells (polyclonal CD4+ T cells and B cells) may be described as being a hallmark of the disease.  These B cells are, in turn, regulated by cells called T follicular helper (Tfh) cells.   While a growing body of evidence points to the crucial roles of Tfh cells in lupus, the mechanism of activation of Tfh cells is currently not well understood.  Preliminary data from Drs. Jarjour and Zhang’s experiments suggest that an enzyme (a ligase) called Cbl-b controls relevant Tfh development in a mouse model of lupus. In the present study, Drs. Jarjour and Zhang will (1) use a mouse model of the illness to investigate further whether and how Cbl-b regulates Tfh cell development.   In addition, (2) they will explore the role of Cbl-b in regulating Tfh cells derived from the blood of lupus patients (with more and less severe illness) and healthy people (to serve as experimental controls). Among the steps Drs. Jarjour and Zhang will take will be to knock down Cbl-b and assess how this step affects the abilities of human Tfh subsets from lupus patients. Further, (3) they will study whether Cbl-b regulates Tfh differentiation in cells derived from humans. 

What this means for people with lupus: Drs. Jarjour and Zhang’s studies are highly focused. Therefore, the possibility exists that this research will lead to the clear identification of therapeutic targets and will facilitate the discovery of lupus therapies. 

Protein S: at the crossroads of thrombosis and inflammation in SLE

Many lupus patients experience abnormal blood clotting and consequent serious consequences for health.  Dr. Rothlin has been investigating a protein that functions in healthy people to inhibit clot formation, a protein named Protein S  (PROS1). The rare variants of PROS1 that appear in some lupus patients impair the anticoagulation function of PROS1, and it may be that  PROS1 mutations affecting blood clotting constitute a risk factor in lupus (although this has not been proven). Previously, some of these same variants had been found in people with blood clotting diseases.  Recently, Dr. Rothlin has shown that PROS1 not only affects blood clotting but is, as well, a potent anti-inflammatory molecule: It inhibits the immune response.  However, whether mutations in PROS1 alter its anti-inflammatory function and thereby contribute to autoimmunity in lupus patients is unknown. She hypothesizes that both the loss of PROS1’s anticoagulant function and the loss of its anti-inflammatory signaling role each contribute independently to the etiology of lupus – and, furthermore, that when both of these inadequacies appear together the risk of lupus and of the development of a more serious form of the disease is exacerbated. Her current project will (1) characterize both the anticoagulant and anti-inflammatory functions of rare PROS1 variants derived from the blood of lupus patients and (2) in a mouse model of lupus determine the direct contribution of the loss of both of these functions of PROS1 to the development of lupus.

What this means for people with lupus:  Dr. Rothlin’s research will explore the relative contribution to the disease mechanism (or mechanisms) of lupus of the two biological properties of Protein S – the effect on clotting and the effect on the immune response.  The findings may help characterize subgroups of lupus patients. (Identifying subgroups of patients is important because, for example, some therapies may be more effective for some patients than for others.)  In addition, her research may guide the design of future lupus therapies related to PROS1 activities. 

Programmed Cell Death 1 and Helios Distinguish TCR-αβ+ Double-Negative (CD4−CD8−) T Cells That Derive from Self-Reactive CD8 T Cells

TCR-αβ+ double-negative (DN; CD4−CD8−) T cells represent a poorly understood cellular subset suggested to contribute to the pathogenesis of the autoimmune disease systemic lupus erythematosus. DN T cells have been proposed to derive from CD8+ cells. However, the conditions that govern the loss of CD8 expression after Ag encounter are unknown. In this study, we tracked the fate of CD8 T cells from transgenic TCR mice exposed to their cognate Ags as self or in the context of infection. We demonstrate that CD8 T cells lose CD8 expression and become DN only when cognate Ag is sensed as self. This process is restricted to tissues where the Ag is present. We also show that DN T cells derived from self-reactive CD8 cells express the inhibitory molecules PD-1 and Helios. These molecules identify a subset of DN T cells in normal mice. A similar population expands when CD8 T cells from repertoires enriched in self-reactive cells (Aire-deficient) are transferred into cognate hosts. Collectively, our data suggest that a subset of DN T cells, identified by the expression of PD-1 and Helios, represent self-reactive cells. Our results provide an explanation for the origin of DN T cells and introduce CD8 loss as a process associated with self-Ag encounter.


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Towards understanding the role of NCF2 in SLE

Scientific Grant Abstract

Recently, Dr. Jacob identified a gene-based risk factor for lupus. The risk factor is called Neutrophil Cytosolic Factor 2 (nicknamed NCF2). NCF2 is part of a protein complex that produces molecules known as reactive oxygen species (ROS). These molecules normally play important, positive roles helping the immune system destroy germs. However, when the genetic code is not perfect, these molecules do not function as they are supposed to function. One consequence of this
is a major decrease in ROS production.

Using cells from people with lupus, he will investigate the functional consequences of reduced production of a protein subunit. In addition, he will study mice with the relevant mutation as a way of looking at how the mutation affects the immune system itself and influences the development

of lupus.

Dr. Jacob’s research is actually seeking to determine whether scientists should alter their basic understanding
of the mechanisms underlying lupus. In other words, his investigations relate to an emerging paradigm shift in our understanding of the disease, whether relevant to all people with lupus or to a subset of people with lupus.

If, as he suspects, the protein complex he is studying helps regulate inflammation and the immune response, then what does this say about the mechanisms that cause the disease? What are the relative roles of pro-inflammatory by-products, regulating responses, and processes designed to limit inflammation? And would somehow boosting levels of certain proteins constitute a path to curbing autoimmunity? 

Targeting interferogenic signals regulated by SLE risk gene PTPN22

Scientific Grant Abstract

Recent studies completed by Dr. Peterson provided new insights into a “risk” gene for lupus, the gene PTPN22. PTPN22 influences signaling in cells important for the immune system, cells that are known as myeloid cells. Preliminary findings suggest that PTPN22 is needed for the efficient production of type 1 interferon. Type 1 interferon has recently been shown to be involved in suppression of inflammation. So, PTPN22 controls both an anti-inflammatory pathway engaged by type 1 interferon and inflammatory factors governed by that pathway. The promoting function of PTPN22 in relation to type 1 interferon involves signaling by Toll-like receptors (TLR) and TRAF-3. TLRs play a critical role in early immune response to invading pathogens. TRAF-3 is a protein important for activation of the type 1 Interferon pathway by the TLRs.

Dr. Peterson has been intrigued by the fact that a variant of PTPN22 named LypW, exhibits reduced function in myeloid cells so that it fails to promote TLR-associated, efficient type 1 interferon. In the immune system, reduced type 1 interferon correlates with elevated production of the inflammatory factor Interleukin (IL)-17. IL-17 is increased in lupus patient’s blood and likely contributes to tissue injury. So, the central hypothesis for Dr. Peterson’s current research is that the LypW variant impairs TLR signaling; which, in turn, impairs myeloid cell production of type 1 interferon. The reduced type 1 interferon leads to increased levels of IL-17, so that excessive inflammation develops and lupus appears. In his current research, Dr. Peterson hopes to discover how PTPN22 impacts human lupus through TLR signaling and type 1 interferon production. He also hopes to identify specific targets for lupus therapy. Furthermore, he hopes to show that people with lupus who have the LypW variant represent a distinct clinical subset of lupus patients, because in these people myeloid signaling and inflammation driven by certain specific factors is somewhat different than they are in other people with lupus. 

Targeting a dendritic cell-stromal axis in lupus

Scientific Grant Abstract

Lymphocytes are cells of the immune system that, when functioning properly, help protect the human body. The lymphoid tissues are the tissues of the human body where lymphocytes are stimulated and autoantibodies generated. A potential way of treating lupus would be to target the infrastructure within the lymphoid tissues, as this infrastructure regulates, directs and helps maintain the lymphocytes. Using a mouse model of lupus, Dr. Lu has recently shown that treatment with a drug, called SU5416 improves T cell function and reduces the level of markers for antibodies associated with lupus. SU5416 can target dendritic cells, which are cells that play a critical role in the regulation of the immune response in humans. Preliminary findings suggest that a function of dendritic cells is to support the lymphoid tissues. Using the same mouse model of lupus, Dr. Lu will, first, test the hypothesis that the dendritic cells affect the lymphoid tissues in ways crucial for lupus; second, that targeting the relationship between dendritic cells and the lymphoid tissue can be used to regulate autoimmune responses. Furthermore, although SU5416 is not approved by the FDA for use in humans, a related drug has been approved by the FDA. This drug, also known as Sutent is called sunitinib (sunitinib used to be called SU11248). So, on the one hand Dr. Lu’s research hopefully will provide insight into how lymphoid tissues are regulated and how the immune response can be controlled. On the other hand, since her research involves a drug already approved by the FDA for humans, there is the potential that the drug might be used for people with lupus. 

Stat3 promotes IL-10 expression in lupus T cells through trans-activation and chromatin remodeling

The immune-regulatory cytokine IL-10 plays a central role during innate and adaptive immune responses. IL-10 is elevated in the serum and tissues of patients with systemic lupus erythematosus (SLE), an autoimmune disorder characterized by autoantibody production, immune-complex formation, and altered cytokine expression. Because of its B cell-promoting effects, IL-10 may contribute to autoantibody production and tissue damage in SLE. We aimed to determine molecular events governing T cell-derived IL-10 expression in health and disease. We link reduced DNA methylation of the IL10 gene with increased recruitment of Stat family transcription factors. Stat3 and Stat5 recruitment to the IL10 promoter and an intronic enhancer regulate gene expression. Both Stat3 and Stat5 mediate trans-activation and epigenetic remodeling of IL10 through their interaction with the histone acetyltransferase p300. In T cells from SLE patients, activation of Stat3 is increased, resulting in enhanced recruitment to regulatory regions and competitive replacement of Stat5, subsequently promoting IL-10 expression. A complete understanding of the molecular events governing cytokine expression will provide new treatment options in autoimmune disorders, including SLE. The observation that altered activation of Stat3 influences IL-10 expression in T cells from SLE patients offers molecular targets in the search for novel target-directed treatment options.

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Role of the BAFF receptor BCMA to control B cell homeostasis and tolerance

Scientific Grant Abstract

T follicular helper (TFH) cells play an important role in the immune system. When they function in a healthy person,
they are critical for the development of protective antibodies
that help fight disease. However, when they are not working correctly the uncontrolled expansion of TFH cells can lead to the production of antibodies that cause autoimmunity. TFH cells cause these harmful antibodies known as ‘autoantibodies’ through the activation of autoreactive B cells, which are B

cells that work against the body of the person who produces them. Relatively little is known about the biology of TFH in lupus or of how autoreactive B cells are activated. Dr. Erickson realized there must be a mechanism through which TFH cell activity is regulated. He suggests a possible way of controlling what happens with TFH as a way of controlling autoantibody production in lupus. His current research focuses on the BAFF cytokine receptor BCMA in the development and function of TFH cells as a way of controlling autoantibody production in lupus. Using lupus-prone mice, he demonstrated that TFH cells express BCMA and another BAFF receptor, called BR3. Furthermore, he demonstrated that the absence of BCMA in T cells enhances TFH accumulation while also permitting BR3 to increase responsiveness to BAFF. Dr. Erickson has identified a new BCMA-BAFF axis that controls TFH homeostasis.

He suggests that the balance between BCMA signaling and BR3 signaling in TFH cells is an important checkpoint in the immune system. BCMA has also been shown to be critical for the development and survival of certain cells known to secrete protective antibodies. Dr. Erickson’s current research will test the novel hypothesis that BCMA signaling may contribute to immune tolerance in lupus by restraining TFH cell expansion and B cell helper activity. He would like to identify the

factors that drive BCMA expression in T cells in people with autoimmunity and hopes to uncover targets that in the future might have a role in lupus therapies. 

Metabolism of Effector T cells as a Target in SLE

Scientific Grant Abstract

It is known that some white blood cells encourage the development of lupus while other white blood cells are protective. Those that encourage the disease include the effector T cells (Teff) while Regulatory T lymphocytes (Treg) can suppress Teff. Dr. Rathmell wants to make use of the fact that the increased activity of white blood cells in people with lupus requires these cells to increase their nutrient consumption and metabolism. He found previously that Teff and Treg utilize and require distinct patterns of metabolism. In other words, the way these cells each build their substance and structure and the way they each generate energy is different. Based on these different metabolic patterns, he hypothesizes that it may be possible to selectively target a metabolic requirement of Teff while sparing or promoting Treg, and that this may permit a new approach to understanding and treating lupus. In particular, the sugar glucose and the metabolism of this sugar are strongly increased in the inflammation inducing effector T lymphocytes (Teff). His current research will explore whether modifying a transporter of a specific sugar will be a way to target metabolic dysfunction so as to impair Teff and promote Treg in lupus. A factor with the scientific nickname NR3b1 can modulate T cell metabolism; while a related factor, NR3b3, has been shown to be a lupus susceptibility factor. Using mouse models he had engineered previously, he will use genetics to test the role of NR3b1 in lupus and also test the effects of a drug that can inhibit the activity of NR3b1 on autoantibody production. He will also test how an inhibitor of a factor called PDHK1 affects the metabolism and activity of Teff and Treg in a mouse model of lupus; for this he will use biochemical tests plus measurement of autoantibodies and lupus disease pathology. Furthermore, he will investigate the metabolism of T cells in lupus and look to identify new aspects that could provide insight or further drug targets in the future. 

KN-93, an inhibitor of calcium/calmodulin-dependent protein kinase IV, promotes generation and function of Foxp3(+) regulatory T cells in MRL/lpr mice

Objective: Foxp3+ regulatory T cells (Treg) are pivotal for the maintenance of peripheral tolerance and prevent development of autoimmune diseases. We have reported that calcium/calmodulin-dependent protein kinase IV (CaMK4) deficient MRL/lpr mice display less disease activity by promoting IL-2 production and increasing the activity of Treg cells. To further define the mechanism of CaMK4 on Treg cells in systemic lupus erythematosus (SLE), we used the Foxp3-GFP reporter mice and treated them with KN-93, an inhibitor of CaMK4. Methods: We generated MRL/lpr Foxp3-GFP mice to record Treg cells; stimulated naïve CD4+ T cells from MRL/lpr Foxp3-GFP mice under Treg polarizing conditions in the absence or presence of KN-93; evaluated the number of GFP positive cells in lymphoid organs and examined skin and kidney pathology at 16 weeks of age. We also examined the infiltration of cells and recruitment of Treg cells in the kidney. Results: We show that culture of MRL/lpr Foxp3-GFP T cells in the presence of KN-93 promotes Treg differentiation in a dose-dependent manner. Treatment of MRL/lpr Foxp3-GFP mice with KN-93 results in a significant induction of Treg cells in the spleen, peripheral lymph nodes and peripheral blood and this is accompanied by decreased skin and kidney damage. Notably, KN-93 clearly diminishes the accumulation of inflammatory cells along with reciprocally increased Treg cells in target organ. Conclusion: Our results indicate that KN-93 treatment enhances the generation of Treg cells in vitro and in vivo highlighting its potential therapeutic use for the treatment of human autoimmune diseases.

RS rearrangement frequency as a marker of receptor editing in lupus and type 1 diabetes - Eline T. Luning Prak

Continued antibody gene rearrangement, termed receptor editing, is an important mechanism of central B cell tolerance that may be defective in some autoimmune individuals. We describe a quantitative assay for recombining sequence (RS) rearrangement that we use to estimate levels of antibody light chain receptor editing in various B cell populations. RS rearrangement is a recombination of a noncoding gene segment in the  antibody light chain locus. RS rearrangement levels are highest in the most highly edited B cells, and are inappropriately low in autoimmune mouse models of systemic lupus erythematosus (SLE) and type 1 diabetes (T1D), including those without overt disease. Low RS rearrangement levels are also observed in human subjects with SLE or T1D.


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Source: Alliance for Lupus Research
Funded Research

Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid (aPL) antibodies - Guillermina Girardi

We developed a new animal model of TMA induced by antiphospholipid (aPL) antibodies, an invaluable tool to understand the molecular and cellular eventsthat determine glomerular endothelial injury. Using this model we found more than one mechanism/signaling pathway is involved in glomerular injury induced by aPL- antibodies. Both complement dependent and complement-independent pathways were identified that lead to glomerular endothelial cell damage and renal function impairment. We also found that C5a-C5aR interaction is a crucial step for the activation of the coagulation cascade and glomerular injury induced by complement activating antibodies. In addition, our studies demonstrated complement independent mechanisms in which reactivity with β2 glycoprotein I (β2GPI) plays an important role in aPL-induced glomerular damage and renal failure. Independently of the mechanism responsible for aPL-induced TMA, mice that express low levels of tissue factor (TF) were protected from glomerular injury.


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Source: Alliance for Lupus Research
Funded Research


Neutrophil Gelatinase Associated Lipocalin As A Biomarker Of Disease Activity In Pediatric Lupus Nephritis - Hermine I. Brunner, MD MSc

To investigate neutrophil gelatinase associated lipocalin(NGAL) concentrations in relation to disease features and worsening of disease activity in pediatric SLE(pSLE), particularly with regard to lupus nephritis.

NGAL in plasma (PNGAL) and urine (UNGAL) were measured by ELISA in 85 participants with pSLE over time (132visits), healthy children (n=50), and children with juvenile idiopathic arthritis (JIA, n=30. pSLE disease features and results of standard laboratory testing were recorded. Disease activity was measured by the systemic lupus disease activity index (SLEDAI-2K).

NGAL in plasm and urine is elevated in pSLE compared to JIA or healthy controls. UNGAL and, to a lesser degree, PNGAL increased with worsening of global, but especially renal disease activity, and may represent novel biomarkers for pSLE. ...

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Source: Alliance for Lupus Research
Funded Research

Maternal lupus and congenital cortical impairment - Bruce T. Volpe

Systemic lupus erythematosus (SLE) is an autoantibody (AAb)-mediated disease that preferentially affects women of childbearing age. Since the offspring of mothers with SLE exhibit a high frequency of learning disorders, we hypothesized that maternally transferred AAbs that bind DNA and the N-methyl-D-aspartate receptor (NMDAR) could play a pathogenic role during fetal brain development. Here we describe a maternal SLE murine model wherein pregnant dams harbored anti-DNA, anti-NMDAR AAbs throughout gestation. High titers of these AAbs in maternal circulation led to histopathological abnormalities in fetal brain and subsequent cognitive impairments in adult offspring. These data support a paradigm in which in utero exposure to neurotoxic AAbs causes abnormal brain development with long-term consequences. This paradigm may apply to multiple congenital neuropsychiatric disorders.

Studies demonstrate that children born to mothers with SLE display a high incidence of learning disorders compared to children born to healthy mothers1-5. In one study as many as 45% of the male and 8% of the female offspring of SLE mothers were affected, generally displaying dyslexia or difficulty with mathematical calculations1. The mechanisms for the learning disorder remain unknown, but prematurity, low birth weight, maternal disease activity, and medications during pregnancy have not emerged as significant causative factors. The striking observation that children born from SLE fathers do not exhibit learning disorders led us to ask whether maternally derived factors, antibodies (Abs) in particular, might alter fetal brain development in utero and result in long-term changes in cognitive function of the offspring.


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Source: Alliance for Lupus Research
Funded Research

Urinary Neutrophil Gelatinase-Associated Lipocalin as a Biomarker of Nephritis in Childhoo-Onset Systemic Lupus Erythematosus - Hermine I. Brunner, MD MSc

Renal involvement in systemic lupus erythematosus (SLE) is associated with poor prognosis.
Currently available renal biomrkers are relatively insensitive and nonspecific for diagnosing SLE nephritis. Previous research suggests that neutrophil gelatinase-associated lipocalin (NGAL)  is a high-quality renal biomarker of acute kidney injury, while its usefulness in SLE is unclear.

We undertook this study to determine the relationship between urinary NGAL excretion and SLE disease activity or damage, with a focus on nephritis.


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Source: Alliance for Lupus Research
Funded Research

Type I Interferon Review in Systemic Lupus Erythematosus and Other Autoimmune Diseases - Virginia Pascual

Different genetic alterations may lead to type I interferon (IFN) overproduction inhuman systemic lupus erythematosus (SLE). The increased bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of immature myeloid dendritic cells (mDCs). IFN-matured mDCs activate autoreactive T cells. These cells, together with plasmacytoid DCs, help expand autoreactive B cells. IFNmatured DCs also activate cytotoxic CD8+ T cells, possibly increasing apoptotic cell availability. The capture of apoptotic cells bymDCs and of nucleic acid-containing immune complexes by plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations. Genetic alterations in lineages other than B cells might explain other autoimmune syndromes where type I IFNs appear to be involved.


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Source: Alliance for Lupus Research
Funded Research

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