Director, Division of Rheumatology and Immunology

Wael Jarjour4505
Vice Chair for Ambulatory Medicine
Martha Morehouse Chair in Arthritis and Immunology Research

480 Medical Centr Dr
Columbus, OH 43210 


Dr. Wael Jarjour Research Lab

Special interests: Dr. Jarjour's specialty interests include rheumatoid arthritis, vasculitis, Lupus, connective tissue diseases and osteoarthritis with research focused on autoimmunity.


Subspecialty training: University of North Carolina at Chapel Hill, 1990
Residency: University Hospital, Milton S. Hershey Medical Center, 1988
Research training: N.I.A.D., National Institutes of Health, 1985
MD: Damascus University, School of Medicine, Damascus, Syria, 1982
Research in the laboratory of Dr. Wael Jarjour

Research in the laboratory of Dr. Wael Jarjour

The research in the laboratory of Dr. Wael Jarjour investigates sex bias in systemic autoimmune disorders and the role of regulatory T cells (Tregs) in myositis and Sjögren’s syndrome.

Systemic Lupus Erythematosus (SLE)

Dr. Jarjour’s laboratory focuses on research activities examining sex bias in lupus and other autoimmune diseases and on how estrogen impacts the immune response. In investigating the role of estrogen receptors and estrogen in SLE and other autoimmune diseases, Dr. Jarjour has demonstrated that estrogen up-regulates numerous genes that regulate the immune response. In recent publications, the team identified two novel targets of estrogen that are significantly up-regulated in SLE patients and play a critical role in regulating inflammation, specifically ZAS3 and TLR8. The research team is currently exploring functional consequences of this up-regulation. The longterm goal of this project is to elucidate the role of estrogen and its receptors in the pathogenesis of SLE and identify biomarkers that will define women who are at high risk of developing lupus. Read our ZAS3 and TLR8 papers.

Another area of research interest for Dr. Jarjour is the development and validation of predictive biomarkers in SLE. To facilitate new collaborative efforts to address this very important translational area, Dr. Jarjour led an international meeting that was held in Washington DC.


Another area of active investigation in the lab concentrates on weakened muscle conditions known as inflammatory myopathies. This group of autoimmune diseases is marked by chronic inflammation of muscle tissue. These inflammatory myopathies are part of a heterogeneous group of diseases with diverse etiologies and clinical manifestations. Importantly, the cause of these diseases remains unclear and could hold the key to understanding the pathogenic mechanisms of autoreactive lymphocyte activation, expansion, and myositic inflammation.

Our work in this area examines the role of Tregs in the development of muscle tissue inflammation through the use and development of novel animal models of these diseases. Specifically, we are examining the interplay between genetics and the environment in promoting an abnormal display of antigens that, in the absence of normal Treg function, allows for the development of myositis. The active role of Tregs in suppressing the inflammatory response of autoreactive cells primed through endogenous antigen exposure has been clearly established in our laboratory. In December 2013, we published Aberrant muscle antigen exposure in mice is sufficient to cause myositis in a Treg cell-deficient milieu and were reviewed here.

Sjögren’s Syndrome

Sjögren’s syndrome is a chronic autoimmune disorder that is caused by persistent inflammation of moisture producing glands. We developed several novel systems to study this disease, including an adoptive transfer model. Recently, our lab has established a chimeric model that displays histological features characteristic of Sjögren’s syndrome pathology. This chimeric model is promising as a system for early drug development to treat Sjögren’s syndrome pathogenesis and progression. Read Novel animal models for Sjögren’s syndrome: Expression and transfer of salivary gland dysfunction from regulatory T cell-deficient mice and A Chimeric Human-Mouse Model Of Sjogren's Syndrome.