Neutrophils in the pathogenesis of systemic autoimmune diseases: casting the NET widely

NIH Director's Seminar Series Systemic autoimmune diseases comprise a clinically heterogeneous group of disorders characterized by a failure in self-tolerance to a wide variety of intracellular autoantigens, and include conditions like systemic lupus erythematosus, rheumatoid arthritis and anti-neutrophil cytoplasmic antibody associated-vasculitis. Work at the Systemic Autoimmunity Branch has focused on characterizing the role that aberrant neutrophils play in the promotion of loss of immunological tolerance, amplification of inflammatory responses and direct end-organ damage in these diseases. One characteristic of neutrophils is their capacity to form neutrophil extracellular traps (NETs) upon exposure to danger signals. Dr. Kaplan's group identified a distinct subset of proinflammatory neutrophils in patients with specific systemic autoimmune diseases (lupus, vasculitis) that display exuberant capacity to form NETs in the absence of infection. She has proposed that NETs may play important roles in the pathogenesis of systemic autoimmune diseases through externalization and modification of intracellular antigens, induction of distinct proinflammatory pathways and deleterious effects on the vasculature and other tissues. Her group has proposed a pathogenic crosstalk between neutrophils and type I IFNs that leads to crucial pro inflammatory pathways in lupus and its associated vascular damage. Dr. Kaplan and her group have identified putative pathways of NET inhibiti...
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