Abstract
Multiple myeloma (MM) is often associated with an increased osteoclast (OC) activity. Using an in vitro osteoclastogenesis model consisting of MM unstimulated and unfractionated peripheral blood mononuclear cells (PBMCs), we showed that T cells support OC formation and survival. Differently, in T cell-depleted MM PBMC cultures, exogenous macrophage-colony stimulating factor (M-CSF) and receptor activated of nuclear factor-kappaB ligand (RANKL) were necessary for osteoclastogenesis. We found RANKL, OPG, and TRAIL overexpression by fresh MM T cells. Despite high osteoprotegerin (OPG) levels, the persistence of osteoclastogenesis can be related to the formation of the OPG/TRAIL complex. Our results highlight that MM T cells support OC formation and survival, possibly involving OPG/TRAIL interaction.
MeSH terms
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Apoptosis Regulatory Proteins / physiology*
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Bone Diseases / etiology
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Bone Diseases / pathology*
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Cells, Cultured
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Female
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Glycoproteins / physiology*
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Humans
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Male
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Membrane Glycoproteins / physiology*
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Models, Biological
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Multiple Myeloma / immunology
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Multiple Myeloma / pathology*
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Osteoclasts / pathology
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Osteoclasts / physiology*
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Osteoprotegerin
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Receptors, Cytoplasmic and Nuclear / physiology*
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Receptors, Tumor Necrosis Factor / physiology*
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Reverse Transcriptase Polymerase Chain Reaction
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T-Lymphocytes / immunology
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TNF-Related Apoptosis-Inducing Ligand
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Tumor Necrosis Factor-alpha / physiology*
Substances
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Apoptosis Regulatory Proteins
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Glycoproteins
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Membrane Glycoproteins
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Osteoprotegerin
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Receptors, Cytoplasmic and Nuclear
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Receptors, Tumor Necrosis Factor
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TNF-Related Apoptosis-Inducing Ligand
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TNFRSF11B protein, human
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TNFSF10 protein, human
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Tumor Necrosis Factor-alpha