東京大学 · 生化学・遺伝学・分子生物学
高屋内教授の研究室は、骨代謝と免疫系のクロスロードに位置する「オステオイムノロジー」を軸に、自己免疫性疾患における骨破壊の分子メカニズムを解明しています。特にRANKLによるオステオクラスト形成の制御機構や、インターフェロンがRANKLシグナルを抑制するシグナルクロスティングのメカニズムに注目し、関節リウマチや骨質疏鯊症の新たな治療標的にふさわしい分子を同定しています。
Figures are computed from collected data and may differ slightly.
RANKL/ODF expressed on synovial fibroblasts is involved in rheumatoid bone destruction by inducing osteoclastogenesis and would therefore be a good therapeutic target.
Osteoclasts are cells of monocyte-macrophage origin that degrade bone matrix. Receptor activator of NF-kappaB ligand (RANKL) induces osteoclast formation in the presence of macrophage-colony-stimulating factor (M-CSF) and costimulatory signals. RANKL induces activation of the TNF receptor-associated factor 6 (TRAF6) and c-Fos pathways, which lead to the osteoclast-specific event, that is, autoamplification of nuclear factor of activated T cells (NFAT)c1, the master transcription factor for osteo
New findings in osteoimmunology will be instrumental in the development of strategies for research into the treatment of various diseases afflicting the skeletal and immune systems.
Regulation of osteoclast differentiation is an aspect central to the understanding of the pathogenesis and the treatment of bone diseases such as autoimmune arthritis and osteoporosis. In fact, excessive signaling by RANKL (receptor activator of nuclear factor kappaB ligand), a member of the tumor necrosis factor (TNF) family essential for osteoclastogenesis, may contribute to such pathological conditions. Here we summarize our current work on the negative regulation of osteoclastogenesis by uni
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