{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T12:14:50Z","timestamp":1778847290225,"version":"3.51.4"},"reference-count":77,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2008,7,1]],"date-time":"2008-07-01T00:00:00Z","timestamp":1214870400000},"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":[[2008,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IL-17 is the hallmark cytokine for the newly identified subset of Th cells, Th17. Th17 cells are important instigators of inflammation in several models of autoimmune disease; in particular, collagen induced arthritis (CIA) and experimental autoimmune encephalomyelitis (EAE), which were previously characterized as Th1-mediated diseases. Although high levels of IFN-\u03b3 are secreted in CIA and EAE, disease is exacerbated in IFN-\u03b3- or IFN-\u03b3 receptor-deficient mice due to the ability of IFN-\u03b3 to suppress IL-17 secretion. However, in proteoglycan-induced arthritis (PGIA), severe arthritis is dependent on the production of IFN-\u03b3. We were therefore interested in determining the role of IL-17 in PGIA. We assessed the progression of arthritis in IL-17-deficient (IL-17\u2212\/\u2212) mice and found the onset and severity of arthritis were equivalent in wild-type (WT) and IL-17\u2212\/\u2212 mice. Despite evidence that IL-17 is involved in neutrophil recruitment, synovial fluid from arthritic joints showed a comparable proportion of Gr1+ neutrophils in WT and IL-17\u2212\/\u2212 mice. IL-17 is also implicated in bone destruction in autoimmune arthritis, however, histological analysis of the arthritic joints from WT and IL-17\u2212\/\u2212 mice revealed a similar extent of joint cellularity, cartilage destruction, and bone erosion despite significantly reduced RANKL (receptor activator of NK-\u03baB ligand) expression. There were only subtle differences between WT and IL-17\u2212\/\u2212 mice in proinflammatory cytokine expression, T cell proliferation, and autoantibody production. These data demonstrate that IL-17 is not absolutely required for autoimmune arthritis and that the production of other proinflammatory mediators is sufficient to compensate for the loss of IL-17 in PGIA.<\/jats:p>","DOI":"10.4049\/jimmunol.181.1.329","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:04:22Z","timestamp":1397847862000},"page":"329-337","source":"Crossref","is-referenced-by-count":84,"title":["Development of Proteoglycan-Induced Arthritis Is Independent of IL-17"],"prefix":"10.1093","volume":"181","author":[{"given":"Paul D","family":"Doodes","sequence":"first","affiliation":[{"name":"Department of Immunology\/Microbiology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yanxia","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Rheumatology, Rush University Medical Center , Chicago, IL 60612"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keith M","family":"Hamel","sequence":"additional","affiliation":[{"name":"Department of Immunology\/Microbiology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yumei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Section of Rheumatology, Rush University Medical Center , Chicago, IL 60612"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Balint","family":"Farkas","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoichiro","family":"Iwakura","sequence":"additional","affiliation":[{"name":"Center for Experimental Medicine, Institute of Medical Science, University of Tokyo , Tokyo,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alison","family":"Finnegan","sequence":"additional","affiliation":[{"name":"Department of Immunology\/Microbiology"},{"name":"Department of Internal Medicine, Section of Rheumatology, Rush University Medical Center , Chicago, IL 60612"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2008,7,1]]},"reference":[{"key":"2026012807101772100_R1","first-page":"55","article-title":"Rheumatoid arthritis","volume-title":"Immunol. 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Leukocyte Biol.","year":"2007"},{"key":"2026012807101772100_R50","first-page":"1129","article-title":"The transcription factor T-bet regulates mucosal T cell activation in experimental colitis and Crohn\u2019s disease","volume-title":"J. Exp. Med.","year":"2002"},{"key":"2026012807101772100_R51","first-page":"5337","article-title":"NF-\u03baB-inducing kinase is a common mediator of IL-17-, TNF-\u03b1-, and IL-1 \u03b2-induced chemokine promoter activation in intestinal epithelial cells","volume-title":"J. Immunol.","year":"1999"},{"key":"2026012807101772100_R52","first-page":"167","article-title":"Complex pattern of Th1 and Th2 activation with a preferential increase of autoreactive Th1 cells in BALB\/c mice with proteoglycan (aggrecan)-induced arthritis","volume-title":"Clin. Exp. 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