Abstract
Tumor necrosis factor (TNF) -inhibitory biological response modifiers include neutralizing antibodies and receptor-immunoglobulin G (IgG) fusion proteins. These agents induce an amelioration of clinical signs and symptoms in most of the patients within a few weeks. Moreover, their inhibitory, or often repairing, effects on joint destruction are further excellent even in Japanese patients receiving a relatively lower dose of methotrexate (MTX) probably due to the direct inhibition of osteoclast activation through TNF.
MeSH terms
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Adalimumab
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Antibodies, Monoclonal / therapeutic use*
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Antibodies, Monoclonal, Humanized
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Antirheumatic Agents / therapeutic use*
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Arthritis, Rheumatoid / drug therapy*
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Arthritis, Rheumatoid / etiology
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Arthritis, Rheumatoid / pathology*
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Disease Progression
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Etanercept
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Humans
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Immunoglobulin G / therapeutic use
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Infliximab
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Joints / pathology*
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Receptors, Tumor Necrosis Factor / therapeutic use*
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Tumor Necrosis Factor-alpha / immunology
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Tumor Necrosis Factor-alpha / physiology*
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antirheumatic Agents
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Immunoglobulin G
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Receptors, Tumor Necrosis Factor
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Tumor Necrosis Factor-alpha
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Infliximab
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Adalimumab
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Etanercept