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): 386-91 PMID29124228show 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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Biochem+Biophys+Rep 2015 ; 4 (ä): 386-91
