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白细胞介素-17与白细胞介素-23：银屑病及其相关合并症作用机制的叙述性综述

Interleukin-17 and Interleukin-23: A Narrative Review of Mechanisms of Action in Psoriasis and Associated Comorbidities.

作者信息

Menter Alan, Krueger Gerald G, Paek So Yeon, Kivelevitch Dario, Adamopoulos Iannis E, Langley Richard G

机构信息

Baylor Scott & White, Dallas, TX, USA.

University of Utah, Salt Lake City, Utah, USA.

出版信息

Dermatol Ther (Heidelb). 2021 Apr;11(2):385-400. doi: 10.1007/s13555-021-00483-2. Epub 2021 Jan 29.

DOI:10.1007/s13555-021-00483-2
PMID:33512665
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8019008/
Abstract

Psoriasis is an immune-mediated inflammatory skin disease associated with numerous inflammatory comorbidities, including increased cardiovascular risk. The interleukin (IL)-23/IL-17 axis plays a central role in the immunopathogenesis of psoriasis and related comorbidities by acting to stimulate keratinocyte hyperproliferation and feed-forwarding circuits of perpetual T cell-mediated inflammation. IL-17 plays an important role in the downstream portion of the psoriatic inflammatory cascade. This review discusses the distinct mechanisms of action of IL-17 and IL-23 in the immunopathogenesis of psoriasis and related comorbidities plus the significant therapeutic benefits of selectively inhibiting these cytokines in patients with moderate to severe plaque psoriasis.

摘要

银屑病是一种免疫介导的炎症性皮肤病，与多种炎症性合并症相关，包括心血管风险增加。白细胞介素（IL）-23/IL-17轴通过刺激角质形成细胞过度增殖和促进持续的T细胞介导的炎症的前馈回路，在银屑病及其相关合并症的免疫发病机制中起核心作用。IL-17在银屑病炎症级联反应的下游部分起重要作用。本综述讨论了IL-17和IL-23在银屑病及其相关合并症免疫发病机制中的不同作用机制，以及选择性抑制这些细胞因子对中度至重度斑块状银屑病患者的显著治疗益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4306/8019008/5666de33a734/13555_2021_483_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4306/8019008/5666de33a734/13555_2021_483_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4306/8019008/5666de33a734/13555_2021_483_Fig1_HTML.jpg

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