اولین همایش بین المللی تحول خدمات سلامت: تلفیق مراقبت، درمان، بازتوانی و امیدبخشی

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کد مقاله 1530

عنوان The Evolving Paradigm of Neutrophil Extracellular Traps (NETs) in Psoriasis Pathogenesis: From Cellular Mechanisms to Targeted Therapies

نویسندگان Nasrin Zare

چکیده Background: IL-23/IL-17 axis has a central role in the pathogenesis of psoriasis, which is a chronic immune-mediated inflammatory skin disorder. Emerging evidence indicates that neutrophils and neutrophil extracellular traps (NETs) play a role in the initiation and propagation of the psoriatic inflammation. This narrative review aims to review the current knowledge regarding the molecular mechanisms involved in NETosis and psoriasis, as well as the new treatment options that are under investigation for the inhibition of NETosis and NET-associated pathways. Methods: PubMed/MEDLINE database was searched for combinations of the following terms: psoriasis, NETs, NETosis, Th17 response, and therapeutic target. Studies directly exploring the link between NETs and psoriasis were given highest priority, both experimentally and clinically. Results: NET formation is higher in psoriatic blood and lesional skin and can lead to activation of keratinocytes and inflammatory responses (1). NET-associated RNA can trigger a self-amplifying inflammatory loop and additional NET release (2), NETs can promote Th17 responses (3), and epidermal NETs can activate epidermal TLR4/IL-36R signaling (4). Recent experimental evidence also suggests that NET formation through PAD4 and STING signaling are involved in macrophage inflammation (5) In the context of obesity-related psoriasis, saturated fatty acids lead to NET formation and to inflammation mediated by IL-17A, and they might decrease responsiveness to anti-IL-17A therapy (6). Conclusions: NETosis is an important aspect of the psoriatic inflammatory network. Most interventions targeted to NETs are still in the preclinical phase, however, and there is a need for biomarkers of NETs and for selective approaches to control pathogenic NET formation, without affecting the function of neutrophils for host defense.

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