| IL-38: A new factor in rheumatoid arthritis Shin-Ichi Takenaka  1 , Shinjiro Kaieda  1 , Tomotaka Kawayama  1 , Masanobu Matsuoka  1 , Yoichiro Kaku  1 , Takashi Kinoshita  1 , Yuki Sakazaki  1 , Masaki Okamoto  1 , Masaki Tominaga  1 , Katsuya Kanesaki  2 , Asako Chiba  3 , Sachiko Miyake  3 , Hiroaki Ida  1 , Tomoaki Hoshino
 Biochem Biophys Rep 
4 
386-391 
2015
 
 Show Abstract
 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-1β 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. | 29124228  |