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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.