Abstract
B cells were originally considered key mediators in the pathogenesis of rheumatoid arthritis (RA). The presence of these cells in many RA synovial tissues and the discovery of rheumatoid factor had put B cells originally at the center of disease pathogenesis. That enthusiasm vanished shortly thereafter only to resurface in the last 15 years with the appearance of highly specific anti-cyclic citullinated protein antibodies. Rituximab, an anti-CD20 antibody that depletes mature B cells, was approved for the treatment of RA in 2006. Since then, B cell depletion strategies have proven efficacy for advanced disease, particularly in those patients that do not respond to DMARDs or TNFα inhibitors.
MeSH terms
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Animals
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Antibodies, Monoclonal, Murine-Derived / administration & dosage
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Antibodies, Monoclonal, Murine-Derived / adverse effects
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Antibodies, Monoclonal, Murine-Derived / therapeutic use*
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Antirheumatic Agents / adverse effects
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Antirheumatic Agents / therapeutic use*
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Arthritis, Rheumatoid / diagnosis
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Arthritis, Rheumatoid / drug therapy*
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Arthritis, Rheumatoid / immunology
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B-Lymphocytes / drug effects*
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B-Lymphocytes / immunology
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Biological Products / adverse effects
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Biological Products / therapeutic use*
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Drug Substitution
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Drug Therapy, Combination
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Humans
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Inflammation Mediators / antagonists & inhibitors
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Inflammation Mediators / metabolism
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Rituximab
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Treatment Outcome
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Tumor Necrosis Factor-alpha / antagonists & inhibitors
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Antibodies, Monoclonal, Murine-Derived
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Antirheumatic Agents
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Biological Products
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Inflammation Mediators
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Tumor Necrosis Factor-alpha
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Rituximab