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However, it remains unclear how dysbiosis enhances Th1 responses, leading to intestinal inflammation. Here, we identified key metabolites derived from dysbiotic microbiota that induce enhanced Th1 responses and exaggerate colitis in mouse models. Patients with CD showed elevated lysophosphatidylserine (LysoPS) concentration in their feces, accompanied by a higher relative abundance of microbiota possessing a gene encoding the phospholipid-hydrolyzing enzyme phospholipase A. LysoPS induced metabolic reprogramming, thereby eliciting aberrant effector responses in both human and mouse IFN-\u03b3\u2013producing CD4+ T cells. Administration of LysoPS into two mouse colitis models promoted large intestinal inflammation. LysoPS-induced aggravation of colitis was impaired in mice lacking P2ry10 and P2ry10b, and their CD4+ T cells were hyporesponsive to LysoPS. Thus, our findings elaborate on the mechanism by which metabolites elevated in patients with CD harboring dysbiotic microbiota promote Th1-mediated intestinal pathology.<\/jats:p>","DOI":"10.1084\/jem.20211291","type":"journal-article","created":{"date-parts":[[2022,5,24]],"date-time":"2022-05-24T15:25:44Z","timestamp":1653405944000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":42,"title":["Lysophosphatidylserines derived from microbiota in Crohn\u2019s disease elicit pathological Th1 response"],"prefix":"10.1084","volume":"219","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8822-9544","authenticated-orcid":true,"given":"Yuriko","family":"Otake-Kasamoto","sequence":"first","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Graduate School of Medicine, Osaka University, Osaka, Japan 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