Targeting tumor necrosis factor α in psoriasis and psoriatic arthritis

Abstract

Background: Psoriasis is an immune-mediated chronic inflammatory disease triggered and maintained by inflammatory mediators, including TNF-α. Objective/methods: To summarize the role of anti-TNF-α agents psoriasis therapy, focusing on the mechanisms and biological pathways involved, by reviewing relevant literature. Results/conclusions: The three TNF-α antagonists currently available (etanercept, infliximab and adalimumab) are effective in the therapy of psoriasis and psoriatic arthritis. Certolizumab pegol and golimumab are TNF-α inhibitors not approved for therapy of psoriasis yet. In addition to neutralizing soluble TNF-α, TNF-α blockers bind to membrane TNF-α and change the behavior of TNF-α-expressing cells, resulting in hastened cell cycle arrest and apopotosis, and suppresion of cytokine production. TNF-α blockers may also affect adaptive immune responses by reducing T helper cell (Th)1 and Th17 responses, and favoring the development of T-regulatory cells. TNF-α antagonists can regulate differentiation and activation of osteoclasts, thus reducing bone destruction in psoriatic arthritis. Anti-TNF-α agents differ in their pharmacokinetics and pharmacodinamic properties, which is reflected in their therapeutic and safety profiles. The safety of TNF-α antagonists has been established, and patient selection and monitoring allow risk minimization.

Keywords::

• adalimumab
• chronic plaque psoriasis
• etanercept
• infliximab
• mechanism of action
• psoriatic arthritis
• TNF-α