T32 Postdoctoral Training Program

Molecular and Translational Rheumatology

Molecular and translational rheumatology is the future dimension of a career in rheumatology at a research university like Columbia. Translational rheumatology involves bringing the rheumatology patient and their disease into the laboratory to unravel the mechanisms responsible for their disease. The goal is simply to understand what is wrong with the patient in molecular terms so that improved and individualized therapies can be developed.

If you are curious about improving understanding of the disease and motivated to improve insight into treatment, then you have what it takes to become a translational rheumatologist. The responsibility of the Division is to provide the training that you need to succeed in this type of an academic career and the principal mechanism for this critical part of your career development is the T32.

Program Mission

The program’s mission is to train promising early career investigators in the methodologies and approaches needed for scientific careers in molecular and translational rheumatology. Eligible candidates are PhD or MD postdoctoral scientists or rheumatology fellows who are committed to autoimmunity research. By providing an innovative training environment that builds on the considerable strengths of Columbia University and supported by a superb set of mentors, we offer three training tracks: genetic predisposition of autoimmunity, mechanisms of rheumatic diseases, and progression to clinical disease.

Program Design

This program consists of one-on-one training by the mentors, as well as required lectures and coursework, and includes optional degree coursework. A major focus of research program is on learning to bridge computational science with the molecular and cellular biology of rheumatic diseases.

Research Mentors 

Anca Askanase, MD, MPH, Professor of Medicine

Dr. Askanase is the associate director of the division of eheumatology and director of rheumatology clinical trials and the Columbia University Lupus Center. Her research in lupus encompasses multiple areas: lupus epidemiology including cohort and registry studies to allow for in depth characterization of disease phenotype and comorbidities, outcomes research to identify biomarkers and develop objective and novel instruments to more accurately diagnose lupus, track disease activity, and define treatment response, and clinical trials to increase treatment options. Much of her research is conducted in collaboration with national and international lupus researchers. She founded the CUIMC Lupus cohort (n=450), and is an active participant in the SLICC and LuCIN registries. She has mentored numerous postdoctoral fellows in lupus-related research projects that fostered their transition to academic careers as rheumatology researchers, and she is the primary mentor for Dr. Gartshteyn, a current Rheumatology post-doctoral fellow who was awarded an KL1 and Daland Fellowship awards. Ongoing projects include the use of optical tomography to evaluate lupus arthritis, development of virtual lupus disease activity measures for use in clinical research, and lupus outreach to disparate populations in NYC.   

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Joan Bathon, MD, Professor of Medicine

Dr. Bathon’s work has focused on understanding the pathogenesis and functional consequences of inflammation in rheumatoid arthritis (RA), particularly the effects of chronic inflammation on the pre-clinical cardiovascular phenotype of RA. Her group comprehensively phenotyped the vascular beds (coronary, carotid, peripheral) of RA patients and identified determinants for accelerated atherosclerosis. Current work uses state-of-the-art cardiac PET/CT scanning to define prevalence, risk factors, and functional consequences associated with pre-clinical myocardial inflammation and microvascular dysfunction in RA. Fundamental to this work has been the assembly of two RA cohorts (ESCAPE ad RHYTHM), complete with biorepositories (DNA, sera, plasma, PBMC), which are extremely well characterized for cardiovascular phenotypes, as well as other extra articular and articular features. These cohorts have been utilized in over 40 published studies, many of them by postdoctoral fellows, and have ignited numerous collaborations since 2004.

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Elana Bernstein, MD, MSc, Assistant Professor of Medicine

Dr. Bernstein’s work focuses on evolution of pre-clinical lung disease in systemic sclerosis (SSc), including the relationship between autoimmunity and interstitial lung disease (ILD). She holds a NIAMS K23 through which she has created a two-institution registry of scleroderma patients (SScREEN ILD) to study the progression of pre-clinical to clinical ILD. She is also one of the PIs of the CONQUER SSc registry, and a site PI of two additional SSc registries (PRESS and GRASP).  She is the site PI for a number of NIH funded clinical trials in scleroderma, and is the program director for the CUIMC / NYP Scleroderma Program. Some of Dr. Bernstein’s major findings include: 1. Patients with subclinical ILD and no clinical ARD have higher serum levels of both IgM rheumatoid factor (RF) and IgA RF than controls without ILD or ARD, supporting a role for autoimmunity in the pathogenesis of ILD. 2. Elucidation for the first time of the survival rates of SSc-ILD patients undergoing lung transplant compared to non-SSc-pulmonary arterial hypertension, and non-SSc-related ILD, patients. 3. Significant global practice variation among SSc experts in screening practices to identify pre-clinical ILD in SSc patients. Her K23 focuses on systematic screening and phenotyping of asymptomatic ILD in SSc, the results of which will inform the development of a clinical practice guideline for ILD screening in SSc. Dr. Bathon is one of the primary mentors for Dr. Bernstein’s K23. Dr. Bernstein has successfully mentored a Rheumatology fellow, resulting in a published manuscript and is currently mentoring a second.

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Angela Christiano, PhD, Professor of Dermatology and Genetics and Development

A major focus of Dr. Christiano’s research is the study of skin and hair disorders in humans and mice, through a classical genetic approach including identification and phenotyping of disease families, genetic linkage, gene discovery and mutation analysis. This work begins by selecting a disorder of interest, then gene discovery, and finally functional studies relating novel proteins to basic questions in epidermal and developmental biology such as cell-cell adhesion, basement membrane zone biology, epidermal differentiation and keratinization or hair follicle morphogenesis and cycling. The laboratory established the genetic and immunologic basis of the autoimmune hair loss disorder, alopecia areata, and pioneered the repurposing of pre-existing, FDA-approved JAK inhibitors to reverse the disease. The pathogenesis of alopecia areata involves many of the same cell populations that are associated with other autoimmune disorders. Through genome wide association studies, genetic similarities were demonstrated between alopecia areata and rheumatoid arthritis with the demonstration of the importance of the HLA-DRB1*04:01 allele and a CTLA-4 polymorphism as major susceptibility genes. This led to a clinical trial of abatacept (CTLA-4-Ig) for the treatment of alopecia areata.

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Hachung Chung, PhD, Assistant Professor in Immunology

Our laboratory is interested in understanding how endogenous (self) RNA sensing by our immune system causes autoimmunity. Pattern recognition receptors (PRRs) are an essential component of the innate immune system responsible for detecting invading pathogens and activating appropriate immunological responses. Many PRRs are specialized in detecting microbial DNA or RNA. Hence, an intriguing question emerges: can PRRs detect endogenous DNA or RNA, and what is the biological significance of self-nucleic acid detection? Indeed, self-nucleic sensing by PRRs is implicated in type I interferonopathies and systemic lupus erythematosus. Moreover, self-nucleic acid sensing by PRRs has also been shown to play a role in neuroinflammation. Our research program focuses on understanding the molecular mechanisms of how self-RNA sensing by PRRs is regulated to prevent autoimmunity. Additionally, we are investigating if enhancement or suppression of self-RNA sensing can be used for immunomodulatory therapies. These studies can help us identify early molecular events that trigger autoinflammation and can lead to discovery of novel RNA therapeutic targets or pathways to treat autoimmunity.

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Remi Creusot, PhD, Assistant Professor of Medical Sciences

Dr. Creusot’s expertise spans 20 years of studying T cell responses in immunity and tolerance, with a focus on the pathogenesis of autoimmune diabetes (T1D). The goal of his research is to understand the mechanisms behind the impaired immune tolerance in T1D and, ultimately, to develop therapeutic approaches to restore long-term immune tolerance. More specifically, his work in autoimmunity involves: 1. Devising and evaluating new approaches for antigen-specific tolerance induction in autoimmune diseases, 2. The generation of humanized mouse models to study the thymic development of human autoreactive T cells and their reactivity to self-antigens in vivo, and 3. Studying stromal, dendritic and NK cells in lymphoid tissues from T1D patients as an investigator in the Network of Pancreatic Organ Donors with Diabetes.

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Christine Garcia, MD, PhD, Professor of Medicine

Dr. Garcia is a molecular geneticist and physician specializing in pulmonary and critical care medicine. Since 2005, she has focused on identifying the genetic underpinnings of idiopathic pulmonary fibrosis (IPF), a lethal scarring lung disease affecting older adults. Her laboratory discovered a number of genes (TERT, TERC, SFTPA2, PARN and RTEL1) linked to familial pulmonary fibrosis and IPF. Unbiased genomic approaches, such as whole genome linkage and whole exome sequencing, have led to the identification of the telomere pathway as being relevant to disease pathogenesis. Her laboratory identified somatic mutations in the telomerase promoter in blood cells that counterbalance inherited telomere-related mutations. She found that peripheral blood leukocyte telomere length is a biomarker of clinically-relevant patient outcomes, such as, survival, rejection after lung transplantation, rate of disease progression as measured by the rate of Forced Vital Capacity decline, and adverse effects of immunosuppressive medications. She currently collaborates with Dr. Bernstein on preclinical and clinical ILD in scleroderma.  

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Laura Geraldino-Pardilla, MD, MS, Associate Professor of Medicine

Dr. Geraldino-Pardilla’s interests focus on cardiovascular disease in RA and SLE, as well as renal involvement in SLE. In RA, she identified risk factors associated with arterial inflammation and circulating antibodies against citrullinated proteins associated with myocardial structural abnormalities and coronary artery calcium scores. In SLE, she has focused on identifying prevalence of electrocardiographic abnormalities and risk factors for clinical and subclinical myocarditis. She is the PI of a local CUIMC SLE CVD Risk Assessment Registry, nested within the larger CUIMC SLE cohort (Askanase, PI) in which CVD risk factors and status are assessed annually in SLE patients. She collaborates with Drs. Winchester, Bathon and Vunjak-Novakovic on a pilot project using cardiac tissue bioengineering to characterize the immune response underlying heart involvement in SLE and RA which is funded currently by the American Heart Association.   

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Ali Gharavi, MD, Professor of Medicine

Dr. Gharavi is the chief of the division of nephrology at CUIMC and interim director of Columbia Institute of Genomic Medicine. He developed a world-class program studying the genetics of complex kidney and urologic traits. One major area of interest is IgA nephropathy (IgAN), the most common glomerulonephritis. His genetic studies have identified new genes and loci for IgAN, and shown shared genetic architecture with multiple immune mediated diseases such as inflammatory bowel disease, celiac disease or rheumatoid arthritis. Dr. Gharavi’s genetic studies have led to the formulation of new pathogenesis model for IgAN, providing the rationale for new clinical trials for this trait. He has trained many students, fellows and young faculty members in investigative medicine, several of whom now have NIH funding. Dr. Gharavi was recipient of the Ewig Clinical Educational Award at CUIMC, and he serves as advisor to several young faculty members on the tenure-track. Dr. Gharavi directed the pre-clinical curriculum in Nephrology for Columbia medical school for the past six years and is the PI of the Columbia nephrology T32 program. He was named the mentor of the year at Columbia University in 2018. 

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Jon Giles, MD, MPH, Associate Professor of Medicine

Dr. Giles is a rheumatologist and epidemiologist with a research focus on understanding the causes and consequences of the articular and non-articular manifestations and comorbidities of various forms of inflammatory arthritis. In rheumatoid arthritis, he has conducted clinical / translational research related to accelerated atherosclerosis, aberrant adipose and muscle composition, novel predictors of interstitial lung disease, and adipokine contributors to erosive joint damage. In psoriatic arthritis, he has conducted studies on adipose tissue inflammation, the genetic basis of phenotypic manifestations, and gene / environment interactions influencing disease phenotype. He is an active investigator in the ESCAPE and RHYTHM cohorts. He is also the PI of an adipose biopsy cohort with stored biospecimens (adipose tissue) and extensive clinical and immunophenotyping data from patients with rheumatoid arthritis, psoriatic arthritis, and healthy controls, funded by a NIAMS R01. A more recently funded NIAMS R01 project is exploring the effect of neuro-activation on tissue inflammation and treatment response in individuals with rheumatoid arthritis. These studies have served as opportunities for research mentoring of more than 15 medical students, residents, and postdoctoral fellows over the last decade, most resulting in publications and, in several, transition to academic research careers. These studies have also resulted in multiple cross-specialty collaborations both within and outside CUIMC that include longstanding relationships with pulmonologists, cardiologists, endocrinologists, radiologists, pathologists, oncologists, and epidemiologists.

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Mark Gorelik, MD, Assistant Professor of Pediatrics 

Dr. Gorelik is an early career faculty member. During his training as his major investigative project, he developed a murine model of Kawasaki disease. He found that a particular mediator of inflammation known as Follistatin Like Protein-1 (FSTL-1) appears to attenuate inflammation in the Kawasaki mouse model and also shows a pattern of expression similar to the mouse in human serum. In addition, FSTL-1 is also known to have therapeutic cardiac effects in mice for function and protection of myocardial tissue when administered exogenously. His current focus is to determine whether treatment with FSTL-1 protein will result in improved cardiac function, decreased damage to myocardial tissue, and decreased overall inflammation in Kawasaki disease and related cardiac inflammatory states. Secondly, he has begun to identify potential mechanisms for this putative protective effect, which appear to be related to modulating immune response. Finally, he has additional data demonstrating potential pathways for intervention in fibrosis for Kawasaki disease and cardiac inflammation. He is currently funded by the American Academy of Allergy, Asthma and Immunology, and a K08 award from the NHLBI. In addition, he also has funding from the Job Research Foundation in investigating the role of STAT3 in fibroblasts in a mouse model of Job Syndrome (STAT3 loss of function). In new collaborations with Drs. Winchester and Novakovic, he is exploring human organoid cardiac models to translate his Kawasaki work to human models. In his prior position, he did not have access to postdoctoral fellows and he looks forward to mentorship of fellows in his current position at CUIMC.

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George Hripcsak, MD, MS, Professor of Biomedical Informatics

Dr. Hripcsak is the Chair of Biomedical Informatics at Columbia University. His research focus is on the clinical information stored in electronic health records and on the development of next-generation health record systems. Using nonlinear time series analysis, machine learning, knowledge engineering, and natural language processing, he is generating evidence for clinical care and developing methods necessary to support clinical research. He leads the Observational Health Data Sciences and Informatics (OHDSI) coordinating center, an international network with 2000 collaborators and 800 million patient records. His 2021 Rheumatology paper characterized autoimmune disease in the setting of COVID-19. In precision medicine, he serves as a PI on Columbia’s eMERGE grant, as a PI on Columbia’s regional recruitment center for the All of Us precision medicine program, and as site PI for Columbia’s role in the All of Us Data and Research Center.

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Clark Hung, PhD, Professor of Biomedical Engineering

Dr. Hung has been pursuing multidisciplinary research using state-of-the-art biological and engineering tools to perform studies to investigate physical effects (e.g., cell deformation, fluid flow effects, osmotic pressure) on cells and tissues comprising the synovial joint. These efforts aim to elucidate the role of joint loading on synovial joint maintenance under normal and pathologic conditions, as well as the utility of applied physiologic loading to foster growth of functional engineered cartilage. Using native or engineered synovium and articular cartilage, his team has developed a biofidelic culture system that captures the natural crosstalk between human joint tissues with applied physiologic loading and cytokine parameters. This model can serve as a platform technology for investigating the role that synovial cells play in joint injury, inflammation as well as healing/repair. Such studies may lead to strategies aimed at alleviating the most prevalent and chronic problems afflicting the musculoskeletal system such as arthritis, and problems related to sports and occupational injuries. 

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Lisa Imundo, MD, Associate Professor of Pediatrics

Dr. Imundo is the past chief of pediatric rheumatology at CUIMC and has a joint appointment in the Departments of Medicine and Pediatrics. In 2014 she was appointed to a joint faculty position in the Department of Medicine in order to develop an innovative program in adolescent rheumatology to transition care from adolescence to young adulthood. She is the PI for multiple Pediatric Rheumatology studies. She was a charter member of the Childhood Arthritis and Rheumatology Alliance and has co-authored 31 important clinical observations from this US-wide pediatric autoimmune registry. She is also an active participant in several other research consortia, including international groups studying TMJ imaging, Juvenile Dermatomyositis, Uveitis and Vasculitis. She served on the American Board of Pediatrics-Rheumatology Sub Board, has been active in the ACR Workforce and Training, Corporate Relations and Government Advocacy committees to improve access and care for children with autoimmune diseases. She is the past president of the Rheumatology Subcommittee at the American Academy of Pediatrics and serves on the executive Committee of Pediatric Specialists. Dr. Imundo has mentored and trained nine post-doctoral trainees including one MD and one MD-PhD candidate.

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Ian Kronish, MD, MPH, Associate Professor of Medicine

Dr. Kronish is a clinical researcher with a research focus on the intersection of psychosocial factors and cardiovascular disease. A focus of his research has been the development of N-of-1 trials, called Personalized Trials, to increase therapeutic precision for hypertension and other common conditions seen in primary care. He directs the NIA-funded Columbia Roybal Center for Fearless Behavior Change which conducts pilot clinical trials aiming to reduce distress and improve health behaviors after acute medical events. His other research explores the contribution of depression and post-traumatic stress disorder to cardiovascular disease outcomes. These projects have served as a context for an extensive experience in the research mentorship of students, residents, and fellows. Dr. Kronish was a mentor for Dr. Runsheng Wang’s K23 in spondyloarthritis. 

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Jose Luchsinger, MD, MPH, Professor of Medicine and Epidemiology

Dr. Luchsinger is a general internist and epidemiologist who has a multidisciplinary research and mentoring program funded by six R01 awards, and a P30 from the NIA. He is also a co-investigator in 2 multisite studies of diabetes treatment and prevention, the Diabetes Prevention Program Outcomes Study (DPPOS), the Glycemia Reduction Approaches in Diabetes (GRADE), in which he leads the study of cognitive and aging outcomes. The research topics covered by his awards include ethnic disparities in medical, vascular, and aging outcomes, the effects of diabetes and pre-diabetes on aging outcomes, the effects of vascular disease on aging outcomes, and the assessment of cognition in primary care settings. Dr. Luchsinger is also the director of the community engagement research core of the Columbia Clinical Translational Science Award (CTSA), which is in charge of engaging the multi-ethnic community of Northern Manhattan in clinical research. Dr. Luchsinger’s research experience includes observational studies, clinical trials, and translational research combining human studies and murine experiments. Dr. Luchsinger has a long history of mentoring, and holds a K24 award.

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Mathew Maurer, MD, Professor of Medicine

The Maurer laboratory focuses on transthyretin (TTR) cardiac amyloidosis and has an active clinical research program evaluating novel methods for treating this condition utilizing TTR stabilizers and gene silencers as well as programs involved in early identification of affected individuals. Dr. Maurer has successfully recruited and retained one of the largest cohorts of patients enrolled in both an observational trial of the natural history of this disorder and an ongoing clinical trial of a novel compound to stabilize the TTR tetramer. He is also co-PI of the NHLBI-funded SCAN-MP study, a collaborative effort between Columbia University and Boston University to utilize nuclear imaging as a screening test of ATTR cardiac amyloidosis in under-represented minority populations. Additionally, he has a current R21 in collaboration with Dr. Giles that is funded by NIA to evaluate patients undergoing clinically indicated lumbar spine surgery for the presence of TTR amyloidosis. He has collaborated with Dr. Winchester on delineating the presence of elevated proportions of circulating activated and effector memory T cells in association with calcific aortic stenosis and the finding of clonal expansions of these T cells in calcified bicuspid and tricuspid aortic valves. Additionally, particularly relevant to this T32, he has founded the Columbia Mentor Peer Aging Research Program (CoMPAdRE), a facilitated peer mentorship program, to foster development of aging research faculties from various disciplines. He holds a K24 award mid-career mentoring award in Geriatric Cardiology from NIA, affirming his commitment to mentoring the next generation of clinician scientist. 

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Joshua Milner, MD, Professor of Pediatrics

Dr. Milner’s work focuses on genetic and immunologic mechanisms of novel and known syndromic causes of atopic disease, immune dysregulation, and primary immune deficiencies. As the chief of the allergy / immunology and rheumatology division in the department of pediatrics, and prior to that of the Laboratory of Allergic Diseases at the NIAID, he has 13 years of experience training clinical fellows in his lab across a wide range of clinical, translational and basic research topics. With a dual appointment in the Institute for Genomic Medicine at CUIMC, he also has access to a wide variety of genomic tools, including patient based next-generation sequencing, to provide broad based research training, including patient-centered projects, mouse models, and in silico, in vivo and in vitro studies.  

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Adam Mor, MD, PhD, Associate Professor of Medicine

Dr. Mor lab’s interest is in studying the signaling events associated with the function of T lymphocytes, with the ultimate goal of developing strategies for the modulation of T cell functions, which will be translated into new therapeutic modalities for patients suffering from cancer and autoimmune diseases. The lab employs advanced techniques to study compartmentalization of signaling events, leveraging conceptually and technologically innovative approaches, combining cutting edge imaging techniques, proteomic and genetic assays, detailed mechanistic studies, powerful computational tools, and inflammatory disease models, all of which work together to propel multidisciplinary strategies. For more information about the research topics of the lab and other training opportunities please refer to:

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Jordan Orange, MD, PhD, Professor and Chairman of Pediatrics

Dr. Orange’s research focuses on understanding which immune system elements enable most individuals to remain healthy despite continuous challenges from our environment. A major focus is the primary immunodeficiencies in which inborn errors of immunity lead to breakdown of the human immune system and subsequent disease. In particular, the laboratory studies human natural killer (NK) cells and their role in maintaining immunity and preventing malignancy. To better understand the requirement for NK cells in health, patients are identified with NK cell deficiencies (NKD) through cutting-edge genetic and genomic technologies. This is complemented by state-of-the-art cell biological techniques to dissect the mechanism by which gene mutations affect NK cell development and function. The lab has significant expertise in modeling patient mutations in NK cell lines, gene editing and microscopy and image analysis, including super-resolution microscopy. Using these approaches, they identified novel NKD including biallelic IRF8deficiency, GATA2 deficiency, MCM10 DEFICIENCY, and FCGR3A mutations as a cause. In addition, his lab actively investigates primary immunodeficiencies that may exhibit NK cell dysfunction, such as Wiskott-Aldrich Syndrome.

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Steve Reiner, MD, Professor of Immunology

Dr. Reiner is the director of the MD-PhD program at CUIMC. His research group has made significant contributions to the understanding of Immunology and Infectious Diseases, most notably demonstrating that lymphocytes act like stem cells to repopulate our immune defense while simultaneously delivering diverse functions that eliminate infectious agents and cancer. One of the ongoing areas of research in the lab which is relevant to this T32 is testing the hypothesis that inhibitory signaling of T cells promotes self-renewal and that blockade of immune checkpoints and expansion protocols for adoptive cell therapy can achieve better durability if agents that promote self-renewal of T cells, particularly those with anti-anabolic properties, are added to standard protocols. 

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Megan Sykes, MD, Professor of Medicine, Immunology, and Surgical Sciences

Dr. Sykes is the director of Columbia Center for Translational Immunology (CCTI). Her major areas of focus are human transplantation immunology, organ allograft tolerance induction, and mechanisms of loss of self-tolerance in autoimmune diseases such as type 1 diabetes and RA. She and her team previously developed novel strategies for achieving graft-versus-tumor effects without graft-versus-host (GVH) disease following hematopoietic cell transplantation (HCT). The Sykes lab also pioneered minimal conditioning approaches for using HCT to achieve organ allograft tolerance. Mechanistic studies have led to an understanding of the roles that anergy and deletion, as well as regulatory cells, play in the allograft tolerance of CD4 and CD8 T cells. The Sykes lab has developed novel “humanized mouse” models that allow personalized analysis of human immune disorders and therapies. These models are currently being used in studies of type 1 diabetes and RA pathogenesis using the “personalized immune” mouse, in which patient-specific immune systems are generated de novo and probed in immunodeficient mice. This approach has been extended to an analysis of thymic selection of autoreactive T cells, through which the lab discovered the preferential positive selection and evasion of negative selection of public T cell receptor hypervariable region sequences that are highly cross-reactive and enriched for autoreactivity. Dr. Sykes has mentored more than 90 scientists, many of whom have become scientific leaders with roles that include professors and department chairs. Her recent studies with Drs. Winchester and Bathon in RA and her understanding of the mechanism of self-tolerance position her as a key mentor for this T32 program. Her research covers both alloreactive and autoreactive immune responses, and her research of the mechanisms by which mixed chimerism reverses autoimmunity is extremely relevant to the themes of this program. Dr. Sykes's ongoing project of sequencing both the T cell and the B cell receptors to distinguish autoimmune recurrence from allograft rejection are very relevant to this T32 program.

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Ira Tabas, MD, PhD, Professor of Medicine and Pathology and Cell Biology and Physiology and Cellular Biophysics

The Tabas laboratory studies the cellular biology of cardiometabolic disease, emphasizing the inflammatory mechanisms of advanced atherosclerosis, hepatic insulin resistance and NASH in obesity, and their links. The atherosclerosis work focuses on macrophage apoptosis, defective clearance of the apoptotic cells (efferocytosis), oxidative stress, and defective inflammation resolution. Studies on hepatic insulin resistance led to the appreciation of a new understanding of adipose tissue inflammation in the setting of obesity and type 2 diabetes (T2D). Ongoing studies are investigating the molecular mechanisms of this new pathway and exploring ways to translate this discovery into new types of drugs to treat T2D and prevent diabetes-driven atherosclerotic plaque progression and inflammation. The overall approach of the laboratory is to elucidate in-depth mechanisms using molecular-cell biological approaches, test causation in normal physiology and disease models using genetically engineered mice, probe relevance to humans through the study of normal and diseased human tissues and human genetics, and conceive and test novel and mechanism-based therapies in the cardiometabolic arena. Dr. Tabas is a recent recipient of the prestigious NIH outstanding investigator R35 award. His expertise in macrophage biology and the association between regulatory T cells and the macrophage efferocytosis during inflammation make him a perfect mentor for this T32. 

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Stavros Thomopoulos, PhD, Professor of Biomechanics

Dr. Thomopoulos joined Columbia University in 2015 as a full professor and the director of the Carroll Laboratories. He specializes in the development, structure-function, repair, and tissue engineering of the tendon-to-bone attachment. He has published numerous papers and one book (Structural Interfaces and Attachments in Biology) on the topic. He leads a laboratory that includes trainees at multiple levels (undergraduates, Ph.D. students, post-doctoral fellows, and staff scientists) and collaborates across multiple schools and departments. Dr. Thomopoulos’ research has been funded by the National Institutes of Health (NIH), the National Science Foundation (NSF), the National Aeronautics and Space Administration (NASA), and the Orthopedic Research and Education Foundation (OREF). He has received numerous awards for his research, including the YC Fung Young Investigator Award from the American Society of Mechanical Engineers, the Neer Award for Basic Science Research in the Shoulder from the American Shoulder and Elbow Surgeons Society, and the Kappa Delta Young Investigator Award from the American Academy of Orthopedic Surgeons.

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Gordana Vunjak-Novakovic, PhD, Professor of Biomedical Engineering

The work in Dr. Vunjak-Novakovic’s Laboratory for Stem Cells and Tissue Engineering is focused on tissue engineering approaches to improving human health. The laboratory has developed a number of innovative technologies for engineering human tissues (e.g., bone, heart) that have been differentiated from induced circulating adult pluripotential stem cells (iPSC) by the integrated use of novel biomaterial scaffolds and bioreactors. The laboratory’s recent successful engineering of in vitro 3D models of relatively mature and functional human cardiac tissue that exhibit adult-like gene expression profiles, organized ultrastructure, and physiology based on the development of iPSC-derived cardiomyocytes from circulating precursors is now being used in collaborative studies with Drs. Winchester, Bathon, Geraldino-Pardilla, and Gorelik to identify immune mechanisms of heart injury in RA, SLE, and Kawasaki disease. The overall hypothesis is that myocardial disease in autoimmune diseases results from targeting cardiac myocytes and other cellular elements in the heart by components of the adaptive autoimmune response, involving either autoantibodies specific for the molecules comprising differentiated heart tissue, and/or by the direct attack of T cells to these target molecules. This collaborative work seeks to model the processes leading to this injury at a molecular and cellular level using autologous mature cardiac tissues generated from iPSCs derived from patients with autoimmune rheumatoid diseases.

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Bob Winchester, MD, Professor of Medicine

The laboratory is organized to study a variety of aspects of how the action of the adaptive immune system results in the development of autoimmune rheumatic diseases. One main direction of the laboratory work concerns the influence of genotype on rheumatic disease development and character of the clinical phenotype. Here a current area of focus is psoriatic arthritis and the influence of HLA-B and HLA-C genotype on the presence and severity of different disease domains such as enthesitis and symmetric or asymmetric sacroiliitis, or on the development of arthritis mutilans. The genotyping uses sequence-based DNA typing performed on a capillary sequencer located in the laboratory. Other genetic work in the laboratory involves determining the extent to which HLA-DR and HLA-DQ alleles or allelicly encoded motifs, such as the shared epitope, influence the development of particular manifestations of rheumatoid arthritis.

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Explore Our Research

For more information on the programs, please contact: 

Bob Winchester, MD
Professor of Medicine

Joan Bathon, MD
Professor of Medicine