オクニシ　カツヒデ   Okunishi Katsuhide   奥西　勝秀    所属   東邦大学  医学部 医学科    職種   教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Hepatocyte growth factor significantly suppresses collagen-induced arthritis in mice.
掲載誌名	正式名：Journal of immunology (Baltimore, Md. : 1950) ISSNコード：0022-1767
掲載区分	国外
出版社	AMER ASSOC IMMUNOLOGISTS
巻・号・頁	179(8),pp.5504-13
著者・共著者	Katsuhide Okunishi,Makoto Dohi,Keishi Fujio,Kazuyuki Nakagome,Yasuhiko Tabata,Takahiro Okasora,Makoto Seki,Mihoko Shibuya,Mitsuru Imamura,Hiroaki Harada,Ryoichi Tanaka,Kazuhiko Yamamoto
発行年月	2007/10/15
概要	Hepatocyte growth factor (HGF) plays an important role in angiogenesis, cell proliferation, antifibrosis, and antiapoptosis. Moreover, recent studies have highlighted the immunosuppressive effect of HGF in animal models of allogenic heart transplantation and autoimmune myocarditis and in studies in vitro as well. We also reported that HGF significantly suppresses dendritic cell function, thus down-regulating Ag-induced Th1-type and Th2-type immune responses in allergic airway inflammation. However, the immunosuppressive effect of HGF in many other situations has not been fully clarified. In the present study, using a mouse model of collagen-induced arthritis (CIA) and experiments in vitro, we examined the effect of HGF on autoimmune arthritis and then elucidated the mechanisms of action of HGF. To achieve sufficient delivery of HGF, we used biodegradable gelatin hydrogels as a carrier. HGF suppressed Ag-induced T cell priming by regulating the functions of dendritic cells in the Ag-sensitization phase with down-regulation of IL-10. In contrast, under continuous Ag stimulation HGF induced IL-10-producing immunocytes both in vivo and in vitro. Moreover, HGF potently inhibited the development of CIA with enhancing the Th2-type immune response. We also confirmed that HGF significantly suppressed the production of IL-17 by immunocytes. These results indicate that HGF suppresses the development of CIA through different ways at different phases. They also suggest that HGF could be an attractive tool for treating patients with rheumatoid arthritis.
DOI	10.4049/jimmunol.179.8.5504
PMID	17911637