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In particular, macrophages and group 2 innate lymphoid cells (ILC2s) are important components of natural immunity that have been shown to play important roles in the pathogenesis of UC, as well as decreased E\u2010cadherin expression on the colonic mucosa. However, it remains unclear how these components interact with each other. In this study, we investigated the molecular mechanisms of UC mediated by macrophage\u2010derived exosomes. We showed for the first time that miR\u201021a\u20105p expression is increased in the peritoneal exosomes of mice with dextran sulphate sodium induced enteritis and that miR\u201021a\u20105p expression correlates negatively with E\u2010cadherin expression in enterocytes. Moreover, we confirmed that miR\u201021a\u20105p was mainly derived from M1 macrophages and demonstrated that KLRG1, a surface inhibitory receptor on ILC2s, participated in excessive ILC2 activation in UC by promoting GATA\u20103. In conclusion, our results suggest molecular targets and provide a theoretical basis for elucidating the pathogenesis of UC and improving its treatment.<\/jats:p>","DOI":"10.1111\/jcmm.16348","type":"journal-article","created":{"date-parts":[[2021,2,11]],"date-time":"2021-02-11T06:22:59Z","timestamp":1613024579000},"page":"3041-3050","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["M1 Macrophage exosomes MiR\u201021a\u20105p aggravates inflammatory bowel disease through decreasing E\u2010cadherin and subsequent ILC2 activation"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8562-5792","authenticated-orcid":false,"given":"Jiaxi","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology Research Center of Digestive Disease The Second XiangYa Hospital Central South University Changsha 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