Abstract
Two cytokines important in the regulation of B-cell function are tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). They act at different steps in B-cell differentiation and can be produced by the B cells themselves upon appropriate stimulation. Crosslinking of surface Ig and signaling through CD22 or CD40 lead to increased secretion of both cytokines. Neutralization of TNF-alpha or IL-6 biologic activity in B-cell cultures results in a significant reduction in B-cell proliferation and Ig secretion. Increased production of these cytokines is found in several diseases associated with aberrant B-cell function. This review will focus on the role of TNF-alpha and IL-6 in normal and pathophysiological conditions of B-cell function.
MeSH terms
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Antibodies, Monoclonal / metabolism
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Antibodies, Monoclonal / pharmacology
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Antigens, CD / immunology
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Antigens, CD / metabolism
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Antigens, Differentiation, B-Lymphocyte / immunology
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Antigens, Differentiation, B-Lymphocyte / metabolism
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B-Lymphocytes / drug effects
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B-Lymphocytes / metabolism*
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CD40 Antigens / metabolism
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Cell Adhesion Molecules*
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Cell Differentiation / drug effects
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Cell Division / drug effects
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Cross-Linking Reagents / metabolism
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Gene Expression Regulation / genetics
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Humans
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Inflammation / metabolism
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Interleukin-6 / metabolism
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Interleukin-6 / pharmacology*
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Lectins*
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Sialic Acid Binding Ig-like Lectin 2
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Signal Transduction / physiology
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Tumor Necrosis Factor-alpha / metabolism
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Tumor Necrosis Factor-alpha / pharmacology*
Substances
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Antibodies, Monoclonal
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Antigens, CD
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Antigens, Differentiation, B-Lymphocyte
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CD22 protein, human
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CD40 Antigens
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Cell Adhesion Molecules
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Cross-Linking Reagents
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Interleukin-6
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Lectins
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Sialic Acid Binding Ig-like Lectin 2
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Tumor Necrosis Factor-alpha