[Mechanism of bone destruction and the contribution of T lymphocytes].
Rheumatoid arthritis (RA), one of the most common autoimmune diseases, is characterized by inflammation and bone destruction in the joints. Abnormal activation of the immune system leads to RANKL-dependent osteoclast differentiation, which ultimately results in bone destruction in RA. A newly identified Th17 subset induces osteoclastogenesis potently by upregulating RANKL on synovial fibroblasts, indicating a synergy between T-synovial fibroblast plays a primary role in the bone destruction. Immune-regulating factors, such as CTLA-4 highly expressed on regulatory T cells, are identified as new bone-regulating factors and can be attractive therapeutic targets for bone destruction in RA. The mechanism by which T cells contribute to the RA pathogenesis will help understand the etiology of RA and develop therapeutic approach against it.
Noriko
N
Komatsu
D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000276:immunology* / Q000473:pathology* / Q000628:therapy; D001842:Bone and Bones / Q000276:immunology* / Q000473:pathology*; D060908:CTLA-4 Antigen / Q000378:metabolism; D002454:Cell Differentiation; D005347:Fibroblasts / Q000502:physiology; D051858:Forkhead Transcription Factors; D006801:Humans; D007596:Joints / Q000276:immunology* / Q000473:pathology*; D058990:Molecular Targeted Therapy; D010010:Osteoclasts / Q000166:cytology / Q000502:physiology; D053245:RANK Ligand / Q000378:metabolism / Q000502:physiology; D013583:Synovial Membrane / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology
D060908:CTLA-4 Antigen; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D053245:RANK Ligand