| First Author | Takenaka SI | Year | 2015 |
| Journal | Biochem Biophys Rep | Volume | 4 |
| Pages | 386-391 | PubMed ID | 29124228 |
| Mgi Jnum | J:351939 | Mgi Id | MGI:7666185 |
| Doi | 10.1016/j.bbrep.2015.10.015 | Citation | Takenaka SI, et al. (2015) IL-38: A new factor in rheumatoid arthritis. Biochem Biophys Rep 4:386-391 |
| abstractText | 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-1beta 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. |
