title: [Cross-talk between immune and skeletal systems].
abstract: Bone destruction in rheumatoid arthritis is characterized as 'the defective control of bone metabolism by the immune system'. During the course of our study to investigate the mechanism of arthritic bone destruction, we have explored a new field called' osteo-immunology'. Here we summarize the regulation of the bone metabolism by signalling cross-talk between RANKL and IFNs, focusing on the T cell-mediated regulation of osteoclastogenesis by IFN-gamma. The better understanding of the interactions between bone and immune cells will provide further insights into the both fields.
authors.affiliation: Department of Immunology, Faculty of Medicine and Graduate School of Medicine, University of Tokyo.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takayanagi
mesh_terms: D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology*; D001862:Bone Resorption; D001842:Bone and Bones / Q000276:immunology / Q000378:metabolism*; D016207:Cytokines / Q000502:physiology; D006023:Glycoproteins / Q000502:physiology; D006801:Humans; D007109:Immunity; D010010:Osteoclasts / Q000502:physiology; D053244:Osteoprotegerin; D011948:Receptors, Antigen, T-Cell; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D006023:Glycoproteins; D053244:Osteoprotegerin; D011948:Receptors, Antigen, T-Cell; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human