Abstract
Soluble decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor superfamily, has recently been reported to increase osteoclast (OC) differentiation. Its impact on the skeleton was reinforced by a study on DcR3 transgenic mice showing a decreased bone mass through the elevation of OC number, providing some initial evidence of DcR3 involvement in bone diseases. In this study we show that malignant plasma cells and T lymphocytes from myeloma patients directly produce DcR3, and this molecule supports the elevated formation of OCs in both peripheral blood and bone marrow from the patients. We also show that serum DcR3 levels in myeloma patients are significantly higher compared to controls.
MeSH terms
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Aged
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Blood Cells / metabolism
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Bone Diseases / blood
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Bone Diseases / metabolism*
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Bone Diseases / pathology
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Bone Diseases / physiopathology
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Case-Control Studies
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Cell Differentiation* / drug effects
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Cells, Cultured
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Female
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Humans
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Male
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Middle Aged
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Multiple Myeloma / blood
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Multiple Myeloma / metabolism*
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Multiple Myeloma / pathology
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Multiple Myeloma / physiopathology
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Osteoclasts / drug effects
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Osteoclasts / physiology*
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Plasma Cells / metabolism
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Plasma Cells / pathology
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RANK Ligand / metabolism
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Receptors, Tumor Necrosis Factor, Member 6b / blood
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Receptors, Tumor Necrosis Factor, Member 6b / metabolism*
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Receptors, Tumor Necrosis Factor, Member 6b / pharmacology
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Receptors, Tumor Necrosis Factor, Member 6b / physiology*
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Solubility
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T-Lymphocytes / metabolism
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T-Lymphocytes / pathology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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RANK Ligand
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Receptors, Tumor Necrosis Factor, Member 6b
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TNFSF11 protein, human
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Tumor Necrosis Factor-alpha