TUMOR NECROSIS FACTOR-α BLOCKADE IN THE TREATMENT OF RHEUMATOID ARTHRITIS
作者： Edward C. Keystone
DOI: 10.1016/S0889-857X(05)70211-8
关键词:
摘要: Tumor necrosis factor-a (TNFa) is a pivotal cytokine in the pathogenesis of rheumatoid arthritis (RA). Several biologic agents have been developed to selectively target this pathogenic element. Infliximab, chimeric mouse/human antiTNFa monoclonal antibody, has shown substantially improve signs and symptoms RA inhibit radiological progression. Etanercept, genetically engineered molecule comprised two human 75kd TNF receptors linked Fc portion immunoglobulin G, demonstrated similar efficacy. New block TNFa developed, including fully antiTNfa PEGylated humanized fragment, soluble p55 receptor. Preclinical data support combination antagonists with providing additive or synergistic effects. A number issues remain unsolved relation antagonists. Despite this, set new therapeutic standard for RA. Further studies are needed clarify their ultimate position algorithm.
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