Abstract
Bone-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.
MeSH terms
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Animals
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Arthritis, Rheumatoid / metabolism*
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Arthritis, Rheumatoid / pathology
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Bone Resorption / physiopathology*
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cell Differentiation
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Cells, Cultured
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Cloning, Molecular
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Cytokines / genetics
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Cytokines / metabolism
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Fibroblasts / metabolism
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Fibroblasts / pathology
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Humans
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Lymphocyte Activation
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / metabolism*
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Mice
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Osteoclasts / metabolism*
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Synovial Membrane / metabolism
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Synovial Membrane / pathology
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism
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T-Lymphocytes / pathology
Substances
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Carrier Proteins
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Cytokines
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Membrane Glycoproteins
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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TNFRSF11A protein, human
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TNFSF11 protein, human
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Tnfrsf11a protein, mouse
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Tnfsf11 protein, mouse