The broad and long-term objectives of the Systemic Autoimmunity Branch are to further the understanding of the pathophysiology and clinical spectrum of systemic autoimmune diseases and to translate this knowledge into better therapies that improve outcomes for patients with these conditions. A major goal of the branch is to combine natural history or treatment studies with basic investigations into the etiology and/or pathophysiology of rheumatic diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).

Additionally, the branch works to train the next generation of scientists and physician-scientists focused on the understanding of the pathogenesis and advancement in the treatments of patients afflicted by systemic autoimmune diseases.

Our research focuses on unraveling fundamental mechanisms underlying immunologic tolerance and understanding innate and adaptive immune pathways crucial to these autoimmune responses in SLE and other autoimmune diseases.

As treatments to suppress aberrant immune responses improve, patients with systemic autoimmunity are able to survive for longer periods of time. As a result, the prevalence of end-stage complications, including the development of accelerated atherosclerosis and myocardial infarction, has increased. We are interested in identifying the immune pathways that promote premature vascular damage in systemic autoimmunity to identify potential preventive strategies.

Current areas of interest

• The role of neutrophils and neutrophil extracellular traps (NETs) in the induction of loss of immunologic tolerance and acceleration of organ and vascular damage in autoimmune diseases.
• How type I Interferons (IFNs) contribute to the development of premature atherogenesis and vasculopathy in SLE and other connective tissue diseases.
• Alterations of immunometabolism in autoimmunity.
• The identification of novel biomarkers and therapeutic targets to mitigate cardiovascular damage and induce immunomodulation in SLE and other systemic rheumatic diseases.