Abstract
The first antibody produced in bacterial or viral infection results from B cell growth as plasmablasts. Dendritic cell-derived TNF-family ligands APRIL and/or BAFF enhance plasmablast survival and differentiation to plasma cells. Expression of these ligands by dendritic cells is promoted by innate immune signals that can convert subliminal B cell activation to a productive response. While this may be lifesaving in the face of infection, it can predispose to autoantibody production.
MeSH terms
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Animals
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Antibody Formation*
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B-Cell Activating Factor
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B-Cell Activation Factor Receptor
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B-Lymphocytes / immunology
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Cell Movement
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Dendritic Cells / immunology*
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Humans
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Ligands
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Lymphocyte Activation
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Lymphocyte Cooperation
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Lymphoid Tissue / immunology
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Membrane Proteins / deficiency
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Membrane Proteins / physiology*
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Mice
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Mice, Knockout
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Mice, Transgenic
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Models, Immunological
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Neuropeptides / physiology*
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Nuclear Proteins / physiology*
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Plasma Cells / immunology
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Receptors, Tumor Necrosis Factor / deficiency
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Receptors, Tumor Necrosis Factor / physiology
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Signal Transduction
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Tumor Necrosis Factor-alpha / deficiency
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Tumor Necrosis Factor-alpha / physiology*
Substances
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ANP32B protein, human
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B-Cell Activating Factor
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B-Cell Activation Factor Receptor
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Ligands
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Membrane Proteins
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Neuropeptides
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Nuclear Proteins
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Receptors, Tumor Necrosis Factor
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TNFRSF13C protein, human
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TNFSF13B protein, human
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Tnfrsf13c protein, mouse
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Tnfsf13b protein, mouse
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Tumor Necrosis Factor-alpha