title: [Mechanism of bone and cartilage damage in rheumatoid arthritis].
abstract: Rheumatoid arthritis(RA)is an autoimmune diseases characterized by inflammation and destruction of bone and cartilage. Bone destruction in RA is triggered by abnormal activation of immune system and osteoclasts induced by RANKL. Advances in osteoimmunology clarified that immune-factors such as inflammatory cytokines and antibodies promote not only inflammation but also bone destruction in RA. Importantly, 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 inflammatory bone destruction. Recently, novel bone-regulating factors are identified and can be attractive therapeutic targets for destruct ion of bone and cartilage in RA.
authors.affiliation: Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Japan.
authors.forename: Noriko
authors.initials: N
authors.lastname: Komatsu
authors.affiliation: Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takayanagi
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001847:Bone Diseases / Q000276:immunology*; D002357:Cartilage Diseases / Q000276:immunology*; D006801:Humans; D010010:Osteoclasts / Q000276:immunology; D053245:RANK Ligand / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D053245:RANK Ligand