PReS-FINAL-2339: Blocking interferon alpha signaling can reduce neutrophil extracellular trap formation in juvenile onset systemic lupus erythematosus

Introduction A novel antimicrobial mechanism of neutrophils involves the release of neutrophil extracellular traps (NETs) into the local environment to bind pathogens. NETs are composed of chromatin, and it has been proposed that a source of autoantigens in Systemic Lupus Erythematosus (SLE) could be increased NETs production. Interferon (IFN)-a is known to be a key player in the pathogenesis of SLE. In Juvenile-onset SLE (JSLE) patients with generally more severe disease, an IFN signature is almost invariably shown at early stages of disease, suggesting that activation of the type-I IFN pathway may be especially important in the induction of the disease process.