Lynch Connor P, Grencis Richard K
The Lydia Becker Institute of Immunology and Inflammation and the Manchester Cell-Matrix Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Parasite Immunol. 2025 Sep;47(9):e70027. doi: 10.1111/pim.70027.
Interleukins 33, 25, and thymic stromal lymphopoietin (TSLP) are core components of type two immune responses and have been studied extensively using helminth infection models. However, many questions remain regarding their cellular sources, their immune recipients, as well as how they shape immunity. Recent literature has demonstrated non-epithelial alarmin production, acting primarily on lymphoid effector cells, and has suggested a role for alarmins in licensing of effector function in tissues during immunity, in dissent with conceptions of classical alarmins as epithelium-derived, myeloid-targeting, and induced prior to adaptive responses. This review examines recent findings in alarmin helminth interactions at barrier sites and discusses the wider implications for how alarmin responses are conceptualised.
白细胞介素33、25和胸腺基质淋巴细胞生成素（TSLP）是2型免疫反应的核心组成部分，并且已经在蠕虫感染模型中得到了广泛研究。然而，关于它们的细胞来源、免疫受体以及它们如何塑造免疫力仍存在许多问题。最近的文献表明存在非上皮性警报素产生，主要作用于淋巴效应细胞，并提示警报素在免疫期间组织中效应功能的许可方面发挥作用，这与经典警报素是上皮来源、靶向髓样细胞且在适应性反应之前诱导产生的概念不同。本综述考察了屏障部位警报素与蠕虫相互作用的最新发现，并讨论了警报素反应概念化的更广泛影响。
