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Dysfunction of ILC3s contributes to the pathogenesis of inflammatory bowel disease (IBD), whereas the mechanisms underlying ILC3 regulation remain incompletely understood. Here, we report that the transcription factor BTB domain and CNC homolog 2 (BACH2) represents an important regulator of intestinal ILC3s. ILC3s from IBD patients exhibited reduced BACH2 expression compared with those from healthy donors. Conditional ablation of BACH2 in ILC3s impaired their function, thereby exacerbating the severity of murine colitis. Mechanistically, BACH2 enhanced mitochondrial oxidative phosphorylation in ILC3s in a peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3)-dependent manner. PPAR\u03b3 was identified as a direct transcriptional target of BACH2 in ILC3s. Notably, pharmacological activation of PPAR\u03b3 with rosiglitazone restored ILC3 function and ameliorated colitis in BACH2-deficient mice. These observations demonstrate that the presence of BACH2-PPAR\u03b3 signaling in ILC3s protects against colitis.<\/jats:p>","DOI":"10.1084\/jem.20251918","type":"journal-article","created":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T06:21:02Z","timestamp":1775542862000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["BACH2 controls ILC3 function via PPAR\u03b3-dependent mitochondrial metabolism"],"prefix":"10.1084","volume":"223","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-3498-2951","authenticated-orcid":true,"given":"Jianye","family":"Wang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02mh8wx89","id-type":"ROR","asserted-by":"publisher"}],"name":"Tianjin Institute of Immunology, School of Basic Medical Sciences, Tianjin Medical University 1 Department of Immunology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), State Key Laboratory of 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