Specific therapy to regulate inflammation in rheumatoid arthritis: Molecular aspects
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Rheumatoid arthritis (RA) is a chronic inflammatory disease in which persistent inflammation of synovial tissue results in a progressive functional decline of the joint and premature mortality. TNF inhibitors were the first biological disease-modifying antirheumatic drugs (DMARDs) used to treat RA. Since then, new biological drugs have emerged, such as inhibitors of IL-1, IL-6 and others, with different mechanisms of action that include the depletion of B cells and the inhibition of T-cell costimulation. Recently, RA treatments have incorporated the use of synthetic DMARDs. This review describes the molecular aspects of the mechanisms of action of biological and synthetic DMARDs, discusses the adverse effects and limitations of established therapies and analyses the alternative approaches to RA treatment. © 2014 Future Medicine Ltd.
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Biological and synthetic agent; Chronic inflammation; Cytokine; Inflammatory response; Molecular aspect; Therapeutic target abatacept; adalimumab; clenoliximab; disease modifying antirheumatic drug; epratuzumab; etanercept; idec 151; infliximab; interleukin 1; interleukin 6; Janus kinase 3; recombinant interleukin 1 receptor blocking agent; rituximab; tocilizumab; tofacitinib; tumor necrosis factor alpha; tumor necrosis factor alpha inhibitor; tumor necrosis factor inhibitor; unclassified drug; antirheumatic agent; IL6 protein, human; interleukin 1; interleukin 6; drug clearance; drug effect; drug half life; drug mechanism; drug receptor binding; human; humoral immune deficiency; inflammation; ligand binding; molecular biology; nonhuman; premature mortality; priority journal; review; rheumatoid arthritis; signal transduction; synovium; T lymphocyte activation; antagonists and inhibitors; Arthritis, Rheumatoid; B lymphocyte; immunology; inflammation; lymphocyte depletion; pathology; T lymphocyte; Antirheumatic Agents; Arthritis, Rheumatoid; B-Lymphocytes; Humans; Inflammation; Interleukin-1; Interleukin-6; Lymphocyte Depletion; T-Lymphocytes
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