title: [Regulation of osteoclastogenesis by activated T cells].
abstract: Bone destruction in rheumatoid arthritis (RA) is caused by osteoclasts, multinuclear cells of the monocyte/macrophage lineage. Since osteoclast differentiation factor RANKL (receptor activator of NF-kappaB ligand) is expressed on activated T cells and T cells, especially Th1 type cells, are implicated in the pathogenesis of RA, it has been believed that they play an important role in the osteoclastogenesis in RA lesions. However, main Th1-type cytokine IFN-gamma strongly suppresses osteoclastogenesis, casting doubt on the relevancy of Th1 cells as stimulators of osteoclastogenesis. Recently, IL-17 from T cells has been reported to enhance osteoclastogenesis. Characterizing real Th subsets which support osteoclastogenesis would be beneficial to solving a clinically important problem, bone destruction in RA.
authors.affiliation: Department of Cell Signaling, Graduate School, Tokyo Medical and Dental University.
authors.forename: Kojiro
authors.initials: K
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takayanagi
mesh_terms: D002454:Cell Differentiation / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D008213:Lymphocyte Activation / Q000502:physiology*; D010010:Osteoclasts / Q000502:physiology*; D013601:T-Lymphocytes / Q000502:physiology*
chemical_list: D016207:Cytokines