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Neutrophil extracellular traps in vasculitis, friend or foe?
Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0002-3328-5060
Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Nephrology.
2018 (English)In: Current Opinion in Rheumatology, ISSN 1040-8711, E-ISSN 1531-6963, Vol. 30, no 1, p. 16-23Article, review/survey (Refereed) Published
Abstract [en]

Purpose of review Neutrophil extracellular traps (NETs) can be found at the sites of vascular lesions and in the circulation of patients with active small vessel vasculitis. Neutrophils from vasculitis patients release more NETs in vitro, and NETs have properties that can harm the vasculature both directly and indirectly. There are several ways to interfere with NET formation, which open for new therapeutic options. However, there are several types of NETs and different mechanisms of NET formation, and these might have different effects on inflammation. Here we review recent findings regarding the pathogenesis and therapeutic potentials of NETs in vasculitis. Recent findings Experimental mouse models support a role for NETs in promoting vascular damage, where histones and mitochondrial DNA appear to be driving forces. Impaired formation of NETs, however, in an SLE-like mouse model leads to more severe disease, suggesting that NETs can be important in limiting inflammation. Studies on drug-induced vasculitis reveal that levamisole can induce NETosis via muscarinic receptors, predisposing for the generation of autoantibodies, including antineutrophil cytoplasmic autoantibodies (ANCA). This supports the notion that NETs can bridge the innate and adaptive immune systems. Summary NETs can participate in the pathogenesis of vasculitis, but in some models there also seem to be protective effects of NETs. This complexity needs further evaluation with experimental models that are as specific as possible for human primary vasculitis.

Place, publisher, year, edition, pages
LIPPINCOTT WILLIAMS & WILKINS , 2018. Vol. 30, no 1, p. 16-23
Keywords [en]
antineutrophil cytoplasmic autoantibodies; autoantigens; inflammation; neutrophil extracellular traps; vasculitis
National Category
Rheumatology and Autoimmunity
Identifiers
URN: urn:nbn:se:liu:diva-147444DOI: 10.1097/BOR.0000000000000450ISI: 000429026200003PubMedID: 28957962OAI: oai:DiVA.org:liu-147444DiVA, id: diva2:1206335
Note

Funding Agencies|Ingrid Asps Foundation; Swedish Society of Nephrology; Swedish Renal Foundation

Available from: 2018-05-16 Created: 2018-05-16 Last updated: 2018-08-03

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Söderberg, DanielSegelmark, Mårten
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Division of Drug ResearchFaculty of Medicine and Health SciencesDepartment of Nephrology
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