Erschienen in:
Open Access
01.12.2012 | Oral presentation
Regulation of inflammatory immune responses leading to the development of bone destructive autoimmune disease rheumatoid arthritis by IL-27
verfasst von:
Takayuki Yoshimoto, Mingli Xu, Izuru Mizuguchi, Yukino Chiba, Sadahiro Kamiya, Masanori Matsui, Shiva Shahrara, Junichiro Mizuguchi
Erschienen in:
Arthritis Research & Therapy
|
Sonderheft 1/2012
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Excerpt
IL-27, a member of the IL-6/IL-12 family of cytokines, induces early helper T (Th)1 differentiation and generation of cytotoxic T cells and IL-10-producing type 1 regulatory T cells, while it suppresses the production of inflammatory cytokines and inhibits Th2 and Th17 differentiation [
1,
2]. The receptor activator of NF-kB ligand (RANKL), which is expressed by not only osteoblasts but also activated T cells, plays an important role in bone-destructive disease rheumatoid arthritis (RA). Recently, IL-17-producing Th17 cells were identified as the exclusive osteoclastogenic T-cell subset. This is because Th17 cells express RANKL, and that IL-17 not only induces RANKL expression on osteoblasts, but also increases the production of various inflammatory molecules. It was previously reported that IL-27 is detected in RA synovial membranes and that treatment with IL-27 attenuated inflammatory responses in collagen-induced arthritis (CIA), one of mouse RA models. …
