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10.1016/j.bbrep.2015.10.015

http://scihub22266oqcxt.onion/10.1016/j.bbrep.2015.10.015
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suck abstract from ncbi


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pmid29124228
      Biochem+Biophys+Rep 2015 ; 4 (ä): 386-391
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  • IL-38: A new factor in rheumatoid arthritis #MMPMID29124228
  • Takenaka SI ; Kaieda S ; Kawayama T ; Matsuoka M ; Kaku Y ; Kinoshita T ; Sakazaki Y ; Okamoto M ; Tominaga M ; Kanesaki K ; Chiba A ; Miyake S ; Ida H ; Hoshino T
  • Biochem Biophys Rep 2015[Dec]; 4 (ä): 386-391 PMID29124228 show ga
  • The newly characterized cytokine IL-38 (IL-1F10) belongs to the IL-1 family of cytokines. Previous work has demonstrated that IL-38 inhibited Candida albicans-induced IL-17 production from peripheral blood mononuclear cells. However, it is still unclear whether IL-38 is an inflammatory or an anti-inflammatory cytokine. We generated anti-human IL-38 monoclonal antibodies in order to perform immunohistochemical staining and an enzyme-linked immunosorbent assay. While human recombinant IL-38 protein was not cleaved by recombinant caspase-1, chymase, or PR3 in vitro, overexpression of IL-38 cDNA produced a soluble form of IL-38 protein. Furthermore, immunohistochemical analysis showed that synovial tissues obtained from RA patients strongly expressed IL-38 protein. To investigate the biological role of IL-38, C57BL/6 IL-38 gene-deficient ((-)(/-)) mice were used in an autoantibody-induced rheumatoid arthritis (RA) mouse model. As compared with control mice, IL-38 ((-/-)) mice showed greater disease severity, accompanied by higher IL-1? and IL-6 gene expression in the joints. Therefore, IL-38 acts as an inhibitor of the pathogenesis of autoantibody-induced arthritis in mice and may have a role in the development or progression of RA in humans.
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