The University of Tokyo · 생화학·유전·분자생물학
히로시 타카야나기 교수의 연구실은 뼈와 면역 시스템의 상호작용을 다루는 온도면역학(osteoinmunology) 분야에서 핵심적인 연구를 수행하고 있습니다. 주로 RANKL/RANK 경로를 중심으로 골다공로시나 자가면역성 관절염과 같은 뼈 질환의 발병 메커니즘을 규명하고, 특히 조혈세포 기원의 골다공로스트의 형성과 조절 메커니즘을 신호 전달 경로와 상호작용 관점에서 연구하고 있습니다. 특히 IFN-γ 등 면역 매개물질이 RANKL 신호를 억제하는 신호 교차 조절 메커니즘을 규명하여 새로운 치료 타겟을 모색하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
