The research in the laboratory of Dr. Wael Jarjour investigates the pathology of systemic autoimmune disorders as influenced by either regulatory T-cells or estrogen.
Autoimmune disease development and progression is a complex process influenced by environmental, hormonal, and genetic factors alike.
Dr. Jarjour participates in his colleagues’ investigations in addition to focusing his research activities on 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 a recent publication, his team identified a novel target of estrogen that is significantly up-regulated in SLE patients and plays a critical role in regulating inflammation. Dr. Jarjour is exploring functional consequences of this up-regulation. The long term goal of this project is elucidating the role of estrogen and its receptors in the pathogenesis of SLE and identifying biomarkers that will define women who are at high risk of developing lupus.
In addition to leading our Division, Dr. Jarjour also is vice chair for Ambulatory Medicine in the Department of Internal Medicine, which has more than 300 faculty members. For the Health and Human Services-funded National Lupus Initiative, Dr. Jarjour is chair of the Lupus Curriculum Review Committee which highlights for U.S. medical school students and residents how health disparities can affect the diagnosis and care of patients with 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.
Another area of active investigation in the lab concentrates on the weakened muscle condition known as myositis. This autoimmune disease 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 of novel animal models of the disease. Regulatory T cells or Tregs are a sub-population of CD4+ T-cells that are responsible for the suppression of auto-reactive T-cell population expansion in the immune system periphery. The active role of Tregs in suppressing the inflammatory response of autoreactive cells primed through endogenous antigen exposure has been clearly established.
Further work in this area will focus on the other complications commonly associated with this disease and will include other novel investigations of Tregs in another autoimmune disorder (Sjogren’s syndrome). The therapeutic application of all this work would ultimately exploit these pathways in patients at risk or with autoimmune disorders and lead to suppression of the disease.