IL-4 和 IL-13:伤口修复的调节因子和效应因子

IF 26.9 1区 医学 Q1 IMMUNOLOGY Annual review of immunology Pub Date : 2023-04-26 Epub Date: 2023-02-03 DOI:10.1146/annurev-immunol-101921-041206
Judith E Allen
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引用次数: 0

摘要

2 型免疫介导对蠕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(包括伤口修复)方面也发挥着广泛的作用。众所周知,2 型细胞因子会促进纤维化,这是一种过度热情的修复反应,但它们对健康伤口修复的贡献却不甚了解。本综述将讨论有证据表明,典型的 2 型细胞因子 IL-4 和 IL-13 通过两条主要途径参与组织修复过程。首先,IL-4 和 IL-13 对有效组织修复的进展至关重要,它们能抑制对损伤的最初炎症反应。其次,这些细胞因子能调节细胞外基质的改变、分解和重建,从而实现有效修复。IL-4和/或IL-13能放大组织修复反应的多个方面,但其中许多途径是高度冗余的,可由其他信号诱导。因此,IL-4Rα 信号传导的确切贡献仍难以揭示。
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IL-4 and IL-13: Regulators and Effectors of Wound Repair.

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.

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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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