The University of Tokyo · Biochemistry, Genetics and Molecular Biology
Professor Hiroshi Takayanagi's research lab specializes in osteoimmunology, focusing on the intricate crosstalk between the immune and skeletal systems. The lab investigates molecular mechanisms underlying osteoclast differentiation and bone destruction, particularly the role of RANKL/RANK signaling and its regulation by interferons and other immune mediators. Key research directions include identifying novel therapeutic targets for autoimmune arthritis, osteoporosis, and other bone-related diseases through detailed dissection of signaling pathways such as NFATc1 autoamplification and TRAF6 activation. The lab also explores how immune cells, especially T cells, contribute to bone homeostasis and pathological bone loss.
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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