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Lung stromal\u2013immune interactions balance pathogen clearance with excessive immune-mediated injury, and healthy lung repair with necessary scarring. Here, we define the lung spatiotemporal stromal-immune response to Influenza A virus (IAV) infection, focusing on the underappreciated role of fibroblasts and their dynamic states. We used 3D quantitative microscopy and scRNAseq to identify IAV-driven fibroblast states, including inflammatory fibroblasts, profibrotic fibroblasts, and adventitial fibroblasts (AFs). Unexpectedly, loss of fibroblast TGF\u03b2 signaling led to early enhancement of immuno-modulatory AFs, driving activation of tissue-resident type 2 regulatory T cells (T2-Tregs) and ultimately improving lung functional outcomes. In vitro co-culture systems additionally revealed that AFs act as a niche to support T2-Tregs. Our data suggest an intimate fibroblast-immune crosstalk is required to temporally and spatially balance lung tissue inflammation and repair.<\/jats:p>","DOI":"10.64898\/2026.04.07.716742","type":"posted-content","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T06:40:12Z","timestamp":1775716812000},"source":"Crossref","is-referenced-by-count":0,"title":["Lung adventitial fibroblasts support type 2 Tregs to shape the response to influenza infection"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6901-3278","authenticated-orcid":false,"given":"Anthony A.","family":"Chang","sequence":"first","affiliation":[{"name":"Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, 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