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However, the detailed mechanism regarding immune regulation by TFF3 is not well defined. Here, we reported that treatment of mouse BM cells and human peripheral blood mononuclear cells from healthy volunteers with TFF3 activated polymorphnuclear myeloid\u2010derived suppressor cells (PMN\u2010MDSCs) in vitro. We also found that prostaglandin E2 is a major TFF3\u2010mediated MDSC target, and that NF\u2010\u03baB\/COX2 signaling was involved in this process. Moreover, TFF3 treatment or transfer of TFF3\u2010derived PMN\u2010MDSCs (TFF3\u2010MDSCs) to experimental necrotizing enterocolitis (NEC) mice caused PMN\u2010MDSC accumulation in the lamina propria (LP), which was associated with decreased intestinal inflammation, permeability, bacterial loading, and prolonged survival. Interestingly, no NEC severity remission was observed in Rag1 KO mice that were given TFF3\u2010MDSCs, but coinjection with CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells significantly relieved NEC inflammation. Overall, TFF3 mediates the NF\u2010\u03baB\/COX2 pathway to regulate PMN\u2010MDSC activation and attenuates NEC in a T\u2010cell\u2010dependent manner, which suggests a novel mechanism in preventing NEC occurrence.\n                  <\/jats:p>","DOI":"10.1002\/eji.202048768","type":"journal-article","created":{"date-parts":[[2021,2,6]],"date-time":"2021-02-06T06:36:13Z","timestamp":1612593373000},"page":"1110-1125","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["TFF3 mediates the NF\u2010\u03baB\/COX2 pathway to regulate PMN\u2010MDSCs activation and protect against necrotizing enterocolitis"],"prefix":"10.1002","volume":"51","author":[{"given":"Jingping","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory The Third Affiliated Hospital of Southern Medical University Southern Medical University  Guangzhou P. R. 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