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IL-4 和 IL-13:伤口修复的调节因子和效应因子。

IL-4 and IL-13: Regulators and Effectors of Wound Repair.

机构信息

Lydia Becker Institute for Immunology and Inflammation and Wellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom; email:

出版信息

Annu Rev Immunol. 2023 Apr 26;41:229-254. doi: 10.1146/annurev-immunol-101921-041206. Epub 2023 Feb 3.

DOI:10.1146/annurev-immunol-101921-041206
PMID:36737597
Abstract

Type 2 immunity mediates protective responses to helminths and pathological responses to allergens, but it also has broad roles in the maintenance of tissue integrity, including wound repair. Type 2 cytokines are known to promote fibrosis, an overzealous repair response, but their contribution to healthy wound repair is less well understood. This review discusses the evidence that the canonical type 2 cytokines, IL-4 and IL-13, are integral to the tissue repair process through two main pathways. First, essential for the progression of effective tissue repair, IL-4 and IL-13 suppress the initial inflammatory response to injury. Second, these cytokines regulate how the extracellular matrix is modified, broken down, and rebuilt for effective repair. IL-4 and/or IL-13 amplifies multiple aspects of the tissue repair response, but many of these pathways are highly redundant and can be induced by other signals. Therefore, the exact contribution of IL-4Rα signaling remains difficult to unravel.

摘要

2 型免疫介导对寄生虫的保护性反应和对过敏原的病理性反应,但它在维持组织完整性方面也有广泛的作用,包括伤口修复。已知 2 型细胞因子可促进纤维化,即过度活跃的修复反应,但它们对健康伤口修复的贡献尚不清楚。这篇综述讨论了证据,即经典的 2 型细胞因子 IL-4 和 IL-13 通过两条主要途径成为组织修复过程的重要组成部分。首先,对于有效的组织修复进展至关重要,IL-4 和 IL-13 抑制损伤后的初始炎症反应。其次,这些细胞因子调节细胞外基质如何被修饰、分解和重建以进行有效的修复。IL-4 和/或 IL-13 放大了组织修复反应的多个方面,但许多这些途径是高度冗余的,并且可以被其他信号诱导。因此,IL-4Rα 信号的确切贡献仍然难以揭示。

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