Abstract
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease with multiple joints involvement. The disease involves inflammation of the synovial membrane, which releases inflammatory cytokines that cause damage to joint components, cartilage and bone, and thus leads to progressive joint destruction. The traditional drugs used for treating RA are known as disease-modifying antirheumatic drugs (DMARDs). The limited efficacy and/or side effects of traditional DMARDs limit their use. Although the etiology of RA remains unknown, recent advances in molecular technology have made it possible to identify distinct cell subsets, cell surface markers, and cell products that contribute to the immune-mediated inflammatory responses associated with the disease. This enhanced understanding of the immunopathogenesis of RA provides opportunities to specifically target the immune response pathways using therapies that are more specific. Over the last decade, five novel biological agents for treatment of RA have already been used in practice or on the horizon: interleukin 1 receptor antagonist (anakinra), anti-TNF agents (infliximab, etanercept, adalimumab), anti-CD20 agent (rituximab), selective T-cell co-stimulation modulator (abatacept), and anti-interleukin 6 receptor (tocilizumab). Here, we briefly discuss the targets of these drugs and the roles of these targets in the pathogenesis of RA and review the efficacy of these drugs from the clinical trial data.
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