Our Lab's Research

• Systemic Lupus Erythematosus (SLE)

  HMGB-1 High Molecular Weight Complexes in SLE

  The Jarjour lab has discovered that proinflammatory protein HMGB1 is a substrate of transglutaminase-2 and forms high-molecular weight complexes with autoantigens. Ongoing work is investigating the composition as well as the formation of this form of HMGB1 in SLE and their contribution to lupus pathogenesis (HMGB-1 High Molecular Weight Complexes in SLE).

  Therapeutic Targeting using neutrophils and microvesicles in SLE

  The Jarjour lab in collaboration with the Lee laboratory is testing novel biochip to transform neutrophils into microscopic vehicles that deliver therapeutic agents to the site of inflammation throughout the body. The study examines the Transfection of Nucleic acids such as microRNA (miRNA) to target inflammatory pathways in lupus nephritis.

• 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. We have demonstrated the role of Tregs in the development of muscle tissue inflammation through the use and development of novel animal models of these diseases (Large functional repertoire). Moreover, our laboratory has developed a myositis mouse model that combines synaptotagmin VII null with FoxP3 mutations, resulting in a mouse with impaired membrane resealing and regulatory T-cell deficiency. This mouse displays robust inflammatory myositis that recapitulate, in part, the human disease (Aberrant Muscle Antigen). Working in collaboration with the Weisleder Laboratory the group has identified antibodies to TRIM72 in patients in myositis patients that compromises cell membrane resealing. This observation lays the ground work for testing if improving membrane resealing could dampen the immune response to muscle proteins in myositis. (Anutoantibodie targeting TRIM72).

• Rheumatoid Arthritis (RA)

  The Jarjour lab in collaboration with Das and Ostrowski labs has been studying various regulators of the inflammatory response in RA Enhancer variants reveal). Moreover, the Jarjour lab (in collaboration with Washington University Roberson lab) is exploring other pathways that can be targeted therapeutically through RNAseq of microRNA, in exosomes isolated from plasma and synovial fluid of patients with RA. Other ongoing research focuses on the development of new therapeutic strategies using mesenchymal stem cells as well as gene regulation in regulatory T cells.

• Sex Bias in Systemic Autoimmune diseases

  Our laboratory studies sex bias in systemic autoimmune disorders with focus on Systemic Lupus Erythematosus (SLE). In investigating the role of estrogen receptors and estrogen in SLE and other autoimmune diseases, our team has identified novel targets of estrogen that are significantly up-regulated in SLE patients and play a critical role in regulating inflammation. 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. Read our ZAS3, TLR8 and Estrogen-regulated STAT1 papers.

• 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 (Novel Animal Models). Our lab has also 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 (A chimeric human).