{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T01:49:36Z","timestamp":1791942576206,"version":"4.3.4"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Liver fibrosis is a severe, life-threatening clinical condition resulting from nonresolving hepatitis of different origins. IL-17A is critical in inflammation, but its relation to liver fibrosis remains elusive. We find increased IL-17A expression in fibrotic livers from HBV-infected patients undergoing partial hepatectomy because of cirrhosis-related early-stage hepatocellular carcinoma in comparison with control nonfibrotic livers from uninfected patients with hepatic hemangioma. In fibrotic livers, IL-17A immunoreactivity localizes to the inflammatory infiltrate. In experimental carbon tetrachloride\u2013induced liver fibrosis of IL-17RA\u2013deficient mice, we observe reduced neutrophil influx, proinflammatory cytokines, hepatocellular necrosis, inflammation, and fibrosis as compared with control C57BL\/6 mice. IL-17A is produced by neutrophils and T lymphocytes expressing the Th17 lineage\u2013specific transcription factor Retinoic acid receptor\u2013related orphan receptor \u03b3t. Furthermore, hepatic stellate cells (HSCs) isolated from naive C57BL\/6 mice respond to IL-17A with increased IL-6, \u03b1-smooth muscle actin, collagen, and TGF-\u03b2 mRNA expression, suggesting an IL-17A\u2013driven fibrotic process. Pharmacologic ERK1\/2 or p38 inhibition significantly attenuated IL-17A\u2013induced HSC activation and collagen expression. In conclusion, IL-17A+ Retinoic acid receptor\u2013related orphan receptor \u03b3t+ neutrophils and T cells are recruited into the injured liver driving a chronic, fibrotic hepatitis. IL-17A\u2013dependent HSC activation may be critical for liver fibrosis. Thus, blockade of IL-17A could potentially benefit patients with chronic hepatitis and liver fibrosis.<\/jats:p>","DOI":"10.4049\/jimmunol.1203013","type":"journal-article","created":{"date-parts":[[2013,7,11]],"date-time":"2013-07-11T00:40:06Z","timestamp":1373503206000},"page":"1835-1844","source":"Crossref","is-referenced-by-count":310,"title":["IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation"],"prefix":"10.1093","volume":"191","author":[{"given":"Zhongming","family":"Tan","sequence":"first","affiliation":[{"name":"Liver Transplantation Center of the First Affiliated Hospital and State Key Laboratory of Reproductive Medicine, Nanjing Medical University , Nanjing, Jiangsu Province 210029,","place":["People\u2019s Republic of China"]},{"name":"The Key Laboratory of Living Donor Liver Transplantation, Ministry of Health , Nanjing 210029,","place":["People\u2019s Republic of China"]},{"name":"Molecular and Experimental 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Republic of China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuehao","family":"Wang","sequence":"additional","affiliation":[{"name":"Liver Transplantation Center of the First Affiliated Hospital and State Key Laboratory of Reproductive Medicine, Nanjing Medical University , Nanjing, Jiangsu Province 210029,","place":["People\u2019s Republic of China"]},{"name":"The Key Laboratory of Living Donor Liver Transplantation, Ministry of Health , Nanjing 210029,","place":["People\u2019s Republic of China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernhard","family":"Ryffel","sequence":"additional","affiliation":[{"name":"Molecular and Experimental Immunology and Neurogenetics-Joint Research Unit 7355, Molecular Immunology, The National Center for Scientific Research-University of Orleans , F-45071 Orleans Cedex 2,","place":["France"]},{"name":"Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town , Rondebosch 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