Abstract
TNF-a is a proinflammatory cytokine known to a have a central role in the initial host response to infection [1–5] and the pathogenesis of various immune-mediated diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus, ankylosing spondylitis (AS), psoriasis (Ps) and/or psoriatic arthritis (PsA), as well as granuloma annulare [1–5]. TNF-a inhibitors have demonstrated efficacy in large, randomized, controlled clinical trials either as monotherapy or in combination with other anti-inflammatory or disease-modifying antirheumatic drugs [1–4]. Five TNF-a inhibitors are available for clinical use: infliximab, adalimumab, golimumab, certolizumab pegol and etanercept [1–5]. Infliximab is a chimeric human/murine IgG1 monoclonal antibody (mAb), adalimumab and golimumab are human mAbs, certolizumab pegol is composed of the Fab antigen-binding domain of a humanized anti-TNF-a mAb combined with polyethylene glycol to increase its half-life in the body and etanercept is a fusion protein that acts as a ‘decoy receptor’ for TNF-a [1–5].
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