Nanke Yuki    Department   School of Nursing, School of Nursing    Position   Professor
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	IL-35 inhibits human osteoclastogenesis from monocytes induced by receptor-activator of NF-κB ligand.
Journal	Formal name：Central-European journal of immunology Abbreviation：Cent Eur J Immunol ISSN code：(1426-3912)1426-3912(Linking)
Domestic / Foregin	Foregin
Volume, Issue, Page	43(2),pp.148-154
Author and coauthor	Yago Toru, Nanke Yuki, Kawamoto Manabu, Kobashigawa Tsuyoshi, Yamanaka Hisashi, Kotake Shigeru
Publication date	2018
Summary	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