{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:35:04Z","timestamp":1791995704844,"version":"4.4.0"},"reference-count":79,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,3,15]]},"abstract":"<jats:p>Idiopathic pulmonary fibrosis (IPF) is a destructive inflammatory disease with limited therapeutic options. To better understand the inflammatory responses that precede and concur with collagen deposition, we used three models of pulmonary fibrosis and identify a critical mechanistic role for IL-17A. After exposure to bleomycin (BLM), but not Schistosoma mansoni eggs, IL-17A produced by CD4+ and \u03b3\u03b4+ T cells induced significant neutrophilia and pulmonary fibrosis. Studies conducted with C57BL\/6 il17a\u2212\/\u2212 mice confirmed an essential role for IL-17A. Mechanistically, using ifn\u03b3\u2212\/\u2212, il10\u2212\/\u2212, il10\u2212\/\u2212il12p40\u2212\/\u2212, and il10\u2212\/\u2212il17a\u2212\/\u2212 mice and TGF-\u03b2 blockade, we demonstrate that IL-17A\u2013driven fibrosis is suppressed by IL-10 and facilitated by IFN-\u03b3 and IL-12\/23p40. BLM-induced IL-17A production was also TGF-\u03b2 dependent, and recombinant IL-17A\u2013mediated fibrosis required TGF-\u03b2, suggesting cooperative roles for IL-17A and TGF-\u03b2 in the development of fibrosis. Finally, we show that fibrosis induced by IL-1\u03b2, which mimics BLM-induced fibrosis, is also highly dependent on IL-17A. IL-17A and IL-1\u03b2 were also increased in the bronchoalveolar lavage fluid of patients with IPF. Together, these studies identify a critical role for IL-17A in fibrosis, illustrating the potential utility of targeting IL-17A in the treatment of drug and inflammation-induced fibrosis.<\/jats:p>","DOI":"10.1084\/jem.20092121","type":"journal-article","created":{"date-parts":[[2010,2,22]],"date-time":"2010-02-22T22:11:58Z","timestamp":1266876718000},"page":"535-552","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":703,"title":["Bleomycin and IL-1\u03b2\u2013mediated pulmonary fibrosis is IL-17A dependent"],"prefix":"10.1084","volume":"207","author":[{"given":"Mark S.","family":"Wilson","sequence":"first","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases 1 , and 2"},{"name":"National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 1 , and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satish K.","family":"Madala","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases 1 , and 2"},{"name":"National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 1 , and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thirumalai R.","family":"Ramalingam","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases 1 , and 2"},{"name":"National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 1 , and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernadette R.","family":"Gochuico","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases 1 , and 2"},{"name":"National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 1 , and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivan O.","family":"Rosas","sequence":"additional","affiliation":[{"name":"Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen W.","family":"Cheever","sequence":"additional","affiliation":[{"name":"Biomedical Research Institute, Rockville, MD 20852 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A.","family":"Wynn","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases 1 , and 2"},{"name":"National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 1 , and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2010,2,22]]},"reference":[{"key":"2023072920371636300_bib1","doi-asserted-by":"crossref","first-page":"494","DOI":"10.4049\/jimmunol.162.1.494","article-title":"IL-17 is produced by nickel-specific T lymphocytes and regulates ICAM-1 expression and chemokine production in human keratinocytes: synergistic or antagonist effects with IFN-gamma and TNF-alpha","volume":"162","author":"Albanesi","year":"1999","journal-title":"J. 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