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 long term 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. 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.

Myositis

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.

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-decient mice and A Chimeric Human-Mouse Model Of Sjogren's Syndrome.

Effects of Stress and Exercise on Lupus Nephritis

Our team is also interested in investigating the effects of stress and exercise on the chronic inflammation associated with autoimmune diseases. We have collaborated with Dr. John Sheridan  and Dr. Sudha Agarwal of the The Ohio State University Wexner Medical Center to investigate the effects of Social Diruption Stress (SDR) and Daily Moderal Exercise (DME) on lupus nephritis in the NZM 2410/J Murine Model, respectively.  Our findings indicate that glomerulonephritis was enhanced with SDR, but significantly improved with DME. Our long term aim is to show that stress reduction and moderate exercise could be used therapeutically in adjunct to pharmacological therapy to help control the chronic inflammation associated with lupus nephritis and other autoimmune diseases.

PubMed list of recent publications