ヤマナカ ヒサシ
  山中 寿
   所属   医学部 医学科(東京女子医科大学病院)
   職種   客員教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 IL-35 inhibits human osteoclastogenesis from monocytes induced by receptor-activator of NF-κB ligand.
掲載誌名 正式名:Central-European journal of immunology
略  称:Cent Eur J Immunol
ISSNコード:(1426-3912)1426-3912(Linking)
掲載区分国外
巻・号・頁 43(2),pp.148-154
著者・共著者 Yago Toru, Nanke Yuki, Kawamoto Manabu, Kobashigawa Tsuyoshi, Yamanaka Hisashi, Kotake Shigeru
発行年月 2018
概要 IL-35 is known as a regulatory cytokine produced by regulatory T cells. It has also been reported that IL-35 suppresses the proliferation of Th17 cells, which is involved in the pathogenesis of many autoimmune diseases. However, in rheumatoid arthritis patients, the role of IL-35 is controversial, and the role of IL-35 in bone metabolism has not been clarified. We investigated the effect of IL-35 on human osteoclast differentiation and activation. We first evaluated the effect of rhIL-35 on human osteoclastogenesis from monocytes cultured alone, induced by soluble-RANKL. We also examined the role of IL-35 on the bone-resorption function of mature osteoclasts. Furthermore, we analysed the molecular mechanism of IL-35 function in monocytes or pre-osteoclasts using RT-PCR. rhIL-35 significantly inhibited human osteoclastogenesis in a dose-dependent manner. In addition, rhIL-35 also significantly decreased the area of pit formation by mature osteoclasts. rhIL-35 significantly decreased mRNA expression of RANK in monocytes and RANK and FOS in pre-osteoclasts. Our current findings suggest that IL-35 inhibits osteoclastogenesis and osteoclast activation by inhibiting both RANK and FOS. IL-35 also has an inhibitory effect on osteoclastic-bone resorption, suggesting that IL-35 may have a therapeutic potential for RA.
DOI 10.5114/ceji.2018.77384
PMID 30135626