{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T19:01:56Z","timestamp":1774119716976,"version":"3.50.1"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T00:00:00Z","timestamp":1398297600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"National Health and Medical Research Council Project","award":["1010563"],"award-info":[{"award-number":["1010563"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,4,24]]},"abstract":"<jats:title>Summary<\/jats:title>\n               <jats:p>Interleukin (IL)-17A is increased both in serum and in kidney biopsies from patients with lupus nephritis, but direct evidence of pathogenicity is less well established. Administration of pristane to genetically intact mice results in the production of autoantibodies and proliferative glomerulonephritis, resembling human lupus nephritis. These studies sought to define the role of IL-17A in experimental lupus induced by pristane administration. Pristane was administered to wild-type (WT) and IL-17A\u2212\/\u2212 mice. Local and systemic immune responses were assessed after 6\u2009days and 8\u2009weeks, and autoimmunity, glomerular inflammation and renal injury were measured at 7\u2009months. IL-17A production increased significantly 6\u2009days after pristane injection, with innate immune cells, neutrophils (Ly6G+) and macrophages (F4\/80+) being the predominant source of IL-17A. After 8\u2009weeks, while systemic IL-17A was still readily detected in WT mice, the levels of proinflammatory cytokines, interferon (IFN)-\u03b3 and tumour necrosis factor (TNF) were diminished in the absence of endogenous IL-17A. Seven months after pristane treatment humoral autoimmunity was diminished in the absence of IL-17A, with decreased levels of immunoglobulin (Ig)G and anti-dsDNA antibodies. Renal inflammation and injury was less in the absence of IL-17A. Compared to WT mice, glomerular IgG, complement deposition, glomerular CD4+ T cells and intrarenal expression of T helper type 1 (Th1)-associated proinflammatory mediators were decreased in IL-17A\u2212\/\u2212 mice. WT mice developed progressive proteinuria, but functional and histological renal injury was attenuated in the absence of IL-17A. Therefore, IL-17A is required for the full development of autoimmunity and lupus nephritis in experimental SLE, and early in the development of autoimmunity, innate immune cells produce IL-17A.<\/jats:p>","DOI":"10.1111\/cei.12287","type":"journal-article","created":{"date-parts":[[2014,2,17]],"date-time":"2014-02-17T11:22:02Z","timestamp":1392636122000},"page":"341-350","source":"Crossref","is-referenced-by-count":40,"title":["Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane"],"prefix":"10.1093","volume":"176","author":[{"given":"S A","family":"Summers","sequence":"first","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"},{"name":"Department of Nephrology, Monash Health, Melbourne, VIC, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D","family":"Odobasic","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M B","family":"Khouri","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"O M","family":"Steinmetz","sequence":"additional","affiliation":[{"name":"III. Medizinische Klinik, Universit\u00e4tsklinikum Hamburg-Eppendorf, Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y","family":"Yang","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S R","family":"Holdsworth","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"},{"name":"Department of Nephrology, Monash Health, Melbourne, VIC, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A R","family":"Kitching","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, VIC, Australia"},{"name":"Department of Nephrology, Monash Health, Melbourne, VIC, Australia"},{"name":"Department of Paediatric 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