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IL-38: A New Factor in Rheumatoid Arthritis

IL-38: A New Factor in Rheumatoid Arthritis

Shin-Ichi Takenaka, Shinjiro Kaieda, Tomotaka Kawayama, Masanobu Matsuoka, Yoichiro Kaku, Takashi Kinoshita, Yuki Sakazaki, Masaki Okamoto, Masaki Tominaga, Katsuya Kanesaki, Asako Chiba, Sachiko Miyake, etc.

Biochem Biophys Rep. 2015 Oct 31;4:386-391.

PMID: 29124228

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413399	IL-38 mouse			Price

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