Allen Judith E, Sutherland Tara E, Rückerl Dominik
Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, United Kingdom.
Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Charlotte Auerbach Road, Edinburgh EH9 3FL, United Kingdom.
Curr Opin Immunol. 2015 Jun;34:99-106. doi: 10.1016/j.coi.2015.03.001. Epub 2015 Mar 18.
The study of immunity to helminth infection has been central to understanding the function of type 2 cytokines and their targets. Although type 2 cytokines are considered anti-inflammatory and promote tissue repair, they also contribute to allergy and fibrosis. Here, we utilise data from helminth infection models, to illustrate that IL-17 and neutrophils, typically associated with pro-inflammatory responses, are intimately linked with type 2 immunity. Neutrophils work with IL-4Rα-activated macrophages to control incoming larvae but this comes at a cost of enhanced tissue damage. Chitinase like proteins (CLPs) bridge these diverse outcomes, inducing both protective IL-17 and reparative Th2 responses. Dysregulation of CLPs, IL-17 and neutrophils likely contribute to disease severity and pathology associated with type 2 immunity.
对蠕虫感染免疫的研究一直是理解2型细胞因子及其靶标功能的核心。尽管2型细胞因子被认为具有抗炎作用并促进组织修复,但它们也会导致过敏和纤维化。在这里,我们利用蠕虫感染模型的数据来说明,通常与促炎反应相关的白细胞介素-17(IL-17)和中性粒细胞与2型免疫密切相关。中性粒细胞与IL-4Rα激活的巨噬细胞协同作用以控制进入的幼虫,但这是以加剧组织损伤为代价的。几丁质酶样蛋白(CLP)连接了这些不同的结果,诱导了保护性的IL-17反应和修复性的辅助性T细胞2(Th2)反应。CLP、IL-17和中性粒细胞的失调可能会导致与2型免疫相关的疾病严重程度和病理变化。