http://orcid.org/0000-0002-2344-1349
![Sample our Bioscience journals, sign in here to start your access, Latest two full volumes FREE to you for 14 days]({"type":"image" , "src" : "/sda/5925/TOC-Subject-Sample-2021-Bioscience.jpg"})
Abstract
Rheumatic diseases are a group of inflammatory conditions that affect joints and connective tissues and are often accompanied by pain and restriction of motility. In many of these diseases, autoantibodies develop that react with molecules/structures commonly found hidden in neutrophils. Neutrophil extracellular trap (NET) formation and release is considered a defense mechanism against pathogens or endogenous danger signals and it has been associated with initial inflammatory responses. NETs are also endowed with an important resolution potential based on its intrinsic enzymatic activity, but in the case they are not timely removed from the crime scene they might modulate subsequent immune responses and contribute to the pathogenesis of chronic inflammatory diseases. In this review, we will summarize the actual knowledge about the multifaceted roles of NETs in the etiology and pathogenesis of rheumatic autoimmune diseases.
Disclosure statement
No potential conflict of interest was reported by the authors.
Figure 1. Various kinds of particulate matter (like bacteria, fungi, viruses or nanoparticles) as well as certain chemicals (LPS, MSU, PMA, ionomycin, bicarbonate and pH) can trigger NET formation. The released NETs then entrap pathogens, sequester necrotic foci and shield wounds; however in pathological conditions they may occlude vessels and ducts. If they are not cleared properly NETs may serve as nucleic acid containing autoantigen that fuel the interferon-driven chronic inflammation a hallmark for systemic lupus erythematosus, SLE.
