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Alan Baer Lab
Research in the Alan Baer Lab focuses on Sjogren's syndrome. Previously, we conducted the Sjogren's International Registry (SICCA), enrolling 300 patients and creating a valuable source of clinical data and biospecimens for research we're conducting with colleagues at Johns Hopkins and the University of California-San Francisco. Currently, we're conducting a longitudinal observational study of patients with Sjogren's syndrome. We're also collaborating with Dr. Ben Larman in the Department of Pathology, using phage immuno-precipation sequencing to work on a characterization of the complete autoantibody repertoire in Sjogren's syndrome patients.
The Ana-Marie Orbai Lab focuses on inflammatory arthritis. Current clinical research projects in the lab examine patient symptoms and experiences in rheumatic diseases and inflammatory arthritis. We focus on stiffness in rheumatoid arthritis and patient-reported outcomes. Previous research in the lab focused on systemic lupus erythemaous (SLE).
Antony Rosen Lab
Research in the Antony Rosen Lab investigates the mechanisms shared by the autoimmune rheumatic diseases such as lupus, myositis, rheumatoid arthritis, scleroderma and SjogrenÕs syndrome. We focus on the fate of autoantigens in target cells during various circumstances, such as viral infection, relevant immune effector pathways and exposure to ultraviolet radiation. Our recent research has sought to define the traits of autoantibodies that enable them to induce cellular or molecular dysfunction. We also work to better understand the mechanisms that form the striking connections between autoimmunity and cancer.
Research in the Dolores Njoku Lab focuses on immune-mediated liver injury caused by drugs such as anti-seizure medications and antibiotics. We use an animal model to understand the pathways involved in the injury process, recognizing that this model can also uncover pathways involved with other drugs that cause similar liver injury. We hope to uncover the immunogenic epitopes, or pieces, of the proteins that trigger the autoimmune reaction and identify the key regulatory pathways involved.
The Erika Darrah Lab is primarily interested in the mechanisms underlying the development and progression of autoimmunity in rheumatoid arthritis (RA), with a particular focus on the peptidyl arginine deiminase (PAD) enzymes. We’re focused on understanding the development of PAD4-activating autoantibodies over time and how they contribute to the development of erosive disease. Studies are underway to determine if the newly discovered antibody is mimicking a naturally occurring PAD4 binding partner and to identify potentially pro-inflammatory effects of citrullinated proteins on effector cells of the immune system.
Felipe Andrade Laboratory
Research in the laboratory of Felipe Andrade, M.D., Ph.D., focuses on the mechanisms of systemic autoimmune diseases, particularly as they relate to the role of cytotoxic granule proteases in autoimmunity and viral clearance, mechanisms of autoantigen citrullination and pathways that control immune effector functions in autoimmune diseases. We currently focus on two principal areas: (1) defining the mechanisms that generate citrullinated autoantigens in vivo in rheumatoid arthritis and (2) understanding the pathways that control the activity of the peptidylarginine deiminase (PAD) enzymes in human neutrophils.
Fredrick Wigley Lab
The Frederick Wigley Lab is interested in the signs, symptoms and causes of scleroderma. We are testing new treatments for RaynaudÕs phenomenon and scleroderma. Understanding the treatment approach to Raynaud's phenomenon and associated ischemia and how to prevent digital ulcers is important for clinicians caring for these patients. Work in our lab has provided guidance in the management of Raynaud's phenomenon and digital ischemic ulcers, including options for the practical pharmacologic and nonpharmacologic interventions.
Investigators in the IBD and Autoimmune Liver Diseases Laboratory conduct basic and translational research in inflammatory bowel disease (IBD) and autoimmune liver diseases. One area of focus is discovering and developing biomarkers for diagnosing and prognosticating IBD and other autoimmune liver diseases (AILDs). We also are exploring the molecular pathogenesis of—and developing novel therapies for—IBD. In addition, we are working to understand the molecular reason why many IBD patients fail to respond to mainstay drug therapies—and to develop diagnostic assays that can predict non-responders before starting them on those therapies. These biomarker studies have led to our application for four U.S. and international patents.
Our research is focused on understanding the basic mechanisms of programmed cell death in disease pathogenesis. Billions of cells die per day in the human body. Like cell division and differentiation, cell death is also critical for normal development and maintenance of healthy tissues. Apoptosis and other forms of cell death are required for trimming excess, expired and damaged cells. Therefore, many genetically programmed cell suicide pathways have evolved to promote long-term survival of species from yeast to humans. Defective cell death programs cause disease states. Insufficient cell death underlies human cancer and autoimmune disease, while excessive cell death underlies human neurological disorders and aging. Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death, particularly in the nervous system, in cancer and in virus infections. Interestingly, cell death regulators also regulate many other cel...lular processes prior to a death stimulus, including neuronal activity, mitochondrial dynamics and energetics. We study these unknown mechanisms.
We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. Natl. Acad. Sci. 94: 690-694, 1997), that cellular anti-death genes can alter the pathogenesis of virus infections (Nature Med. 5:832-835, 1999) and of genetic diseases (PNAS. 97:13312-7, 2000) reflective of many human disorders. We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains. view more
Jean Kim Lab
The Jean Kim Laboratory performs translational research in the
area of chronic rhinosinusitis, with a niche interest in the pathogenesis of hyperplastic nasal
polyposis. Studies encompass clinical research to basic wet laboratory research in
studying the underlying immune and autoimmune mediated mechanism of polyp growth and
perpetuation of disease. Human cell and tissue culture models are used. Techniques in the
laboratory include cell and tissue culture, real time PCR, immunoblot, ELISA, flow cytometry,
immunohistochemistry, electron microscopy, gene array analysis, and other molecular
approaches including genetic knockdowns. Approaches used in Dr. Kim’s clinical study
designs include prospective and retrospective analysis of patient outcomes and clinical
biomarkers, as wells controlled clinical trials.