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.

中文翻译：

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IL-4 和 IL-13：伤口修复的调节因子和效应因子

2 型免疫介导对蠕虫的保护性反应和对过敏原的病理反应，但它在维持组织完整性（包括伤口修复）方面也具有广泛的作用。众所周知，2 型细胞因子会促进纤维化，这是一种过度热切的修复反应，但它们对健康伤口修复的贡献尚不清楚。本综述讨论了以下证据：经典 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 抑制对损伤的初始炎症反应，这对于有效组织修复的进展至关重要。其次，这些细胞因子调节细胞外基质的修饰、分解和重建以实现有效修复。 IL-4 和/或 IL-13 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，并且可以由其他信号诱导。因此，IL-4Rα 信号传导的确切贡献仍然难以阐明。