Neutrophils in Inflammation and Autoimmunity

Neutrophils are instrumental in host defense – however exaggerated neutrophil activation can cause inflammation, organ damage and autoimmunity, including rheumatic disease. Upon neutrophil death, including neutrophil extracellular trap formation, neutrophil extrude mitochondria into the extracellular environment where they can promote inflammation as well as serve as an immunogen for the formation of anti-mitochondrial antibodies. Levels of neutrophil activation markers, as well as extracellular mitochondria are highly elevated in various inflammatory rheumatic diseases, corresponding to disease activity and severity. This presentation will highlight key mechanisms involved in driving neutrophil activation in rheumatic diseases, discuss potential therapeutic targets, while also describing the clinical utility of measuring neutrophil-derived biomarkers and mitochondrial fragments and autoantibodies in a clinical lab setting. After viewing this lecture, participants should be able to: 1. Describe key neutrophil effector functions contributing to inflammation. 2. Consider neutrophil-derived biomarkers in diagnosis and prognosis of rheumatic diseases. 3. Discuss the role of extracellular mitochondria in inflammation. Christian Lood, PhD Associate Professor, Rheumatology Department of Medicine University of Washington 02/18/26 The University of Washington is committed to ensuring digital accessibility in our services, programs, and activities. If you encounter accessibility barriers using videos found on this channel, please contact UW Video at uwvideo [at] uw [dot] edu.