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We found that IFN-\u03bb is a profibrotic factor that is upregulated in fibrotic human and mouse kidneys. IFN-\u03bb receptor deficiency ameliorated renal fibrosis in mice while exogenous IFN-\u03bb exacerbated disease, establishing a detrimental role of IFN-\u03bb signaling in renal fibrosis. Mechanistically, we found that IFN-\u03bb promotes fibrosis by preferentially acting on renal fibroblasts, inducing their activation and migration through ERK\/JNK-dependent synthesis of TGF-\u03b2 and activation of the TGF-\u03b2-SMAD2\/3 signaling pathway. Renal tubular epithelial cell (TEC)-derived IFN-\u03bb induced by RIG-I\/MAVS signaling emerged as a critical driver of renal fibroblast activation and fibrogenesis. Importantly, neutralizing antibodies against IFN-\u03bb strongly attenuated renal fibrosis in mice. Thus, the renal TEC\u2013IFN-\u03bb\u2013fibroblast axis is a previously unrecognized pathway of renal fibrosis induction that represents an attractive novel target for mitigating CKD progression.<\/jats:p>","DOI":"10.1084\/jem.20251858","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T14:15:20Z","timestamp":1783347320000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Interferon-\u03bb drives renal fibrosis by coordinating epithelial\u2013fibroblast crosstalk"],"prefix":"10.1084","volume":"223","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8747-0678","authenticated-orcid":true,"given":"Yunfeng","family":"Zhou","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01vy4gh70","id-type":"ROR","asserted-by":"publisher"}],"name":"School of Basic Medical Sciences, International Cancer Center, Shenzhen University Medical School, Shenzhen University 1 Guangdong 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