[Bone and cartilage destruction in rheumatoid arthritis].
Rheumatoid arthritis is an inflammation-mediated bone disease characterized by local joint inflammation which results from systemic immune responses. It is essential to clarify the mechanisms by which inflammation elicits bone destruction for the establishment of novel therapeutic strategies. Advances in osteoimmunology, in addition to the development of a various kind of genetically-modified mice and animal models of RA, have greatly contributed to our understanding of these mechanisms. Recently, Th17 cells have been shown to contribute not only to the initiation and amplification of inflammation in RA, but also to bone destruction by enhancing osteoclast differentiation through the interaction with synovial fibroblasts. Thus, Th17-synovial fibroblasts interaction is considered to be a promising therapeutic target for RA.
Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo/Global Center of Excellence (GCOE) Program, International Research for Molecular Science in Teeth and Bone Diseases, Japan.
Noriko
N
Komatsu
Hiroshi
H
Takayanagi
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology* / Q000628:therapy; D001842:Bone and Bones / Q000276:immunology / Q000473:pathology*; D002356:Cartilage / Q000276:immunology / Q000473:pathology*; D002454:Cell Differentiation; D005347:Fibroblasts / Q000276:immunology / Q000502:physiology; D006801:Humans; D051379:Mice; D058990:Molecular Targeted Therapy; D010010:Osteoclasts / Q000166:cytology / Q000276:immunology; D053245:RANK Ligand; D013583:Synovial Membrane / Q000166:cytology; D058504:Th17 Cells / Q000276:immunology / Q000502:physiology
D053245:RANK Ligand