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Endogenous interleukin ( IL)-17 A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane.
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- Author(s): Summers, S. A.; Odobasic, D.; Khouri, M. B.; Steinmetz, O. M.; Yang, Y.; Holdsworth, S. R.; Kitching, A. R.
- Source:
Clinical & Experimental Immunology; Jun2014, Vol. 176 Issue 3, p341-350, 10p- Subject Terms:
- Source:
- Additional Information
- Abstract: Interleukin ( IL)-17 A 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-17 A in experimental lupus induced by pristane administration. Pristane was administered to wild-type ( WT) and IL-17 A−/− mice. Local and systemic immune responses were assessed after 6 days and 8 weeks, and autoimmunity, glomerular inflammation and renal injury were measured at 7 months. IL-17 A production increased significantly 6 days after pristane injection, with innate immune cells, neutrophils ( Ly6 G+) and macrophages ( F4/80+) being the predominant source of IL-17 A. After 8 weeks, while systemic IL-17 A was still readily detected in WT mice, the levels of proinflammatory cytokines, interferon ( IFN)-γ and tumour necrosis factor ( TNF) were diminished in the absence of endogenous IL-17 A. Seven months after pristane treatment humoral autoimmunity was diminished in the absence of IL-17 A, with decreased levels of immunoglobulin ( Ig)G and anti-ds DNA antibodies. Renal inflammation and injury was less in the absence of IL-17 A. 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-17 A−/− mice. WT mice developed progressive proteinuria, but functional and histological renal injury was attenuated in the absence of IL-17 A. Therefore, IL-17 A 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. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Clinical & Experimental Immunology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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