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The molecular mechanism of osteoclastogenesis in rheumatoid arthritis Udagawa N; Kotake S; Kamatani N; Takahashi N; Suda TArthritis Res 2002[]; 4 (5): 281-9Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte-macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-kappaB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte-macrophage colony-stimulating factor and IFN-gamma, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.|Animals[MESH]|Arthritis, Rheumatoid/*metabolism/pathology[MESH]|Bone Resorption/*physiopathology[MESH]|Carrier Proteins/genetics/*metabolism[MESH]|Cell Differentiation[MESH]|Cells, Cultured[MESH]|Cloning, Molecular[MESH]|Cytokines/genetics/metabolism[MESH]|Fibroblasts/metabolism/pathology[MESH]|Humans[MESH]|Lymphocyte Activation[MESH]|Membrane Glycoproteins/genetics/*metabolism[MESH]|Mice[MESH]|Osteoclasts/*metabolism[MESH]|RANK Ligand[MESH]|Receptor Activator of Nuclear Factor-kappa B[MESH]|Synovial Membrane/metabolism/pathology[MESH]|T-Lymphocytes/immunology/metabolism/pathology[MESH] |
