Infliximab is a chimeric human-mouse IgG that binds to tumor necrosis factor alpha (TNF-α) and blocks its activity.
Psoriasis vulgaris is an inflammatory skin disease that occurs in ~1-3% of the population. Its pathogenesis is multifactorial and includes environmental, autoimmune, and genetic influences. Psoriatic arthritis (PsA) is a rheumatoid factor-seronegative inflammatory arthritis that is associated with psoriasis. Most patients with PsA develop the arthritic symptoms years after developing cutaneous lesions, but some can develop joint symptoms upfront. Any joint can be affected, and patients typically present with joint pain, stiffness, and/or swelling. Treatment includes non-steroid anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), TNF-inhibitors, and immunosuppressants.
Infliximab is indicated in patients with moderate to severe PsA and acts by binding to TNF-α and blocking its activity. TNF-α promotes systemic inflammation by inducing proinflammatory cytokines (e.g., IL-1 and IL-6), facilitating leukocyte migration from blood vessels into the tissues and increasing the release of adhesion molecules.
Efalizumab is a monoclonal antibody that inhibits lymphocyte activation and cell migration by binding to CD11a. It was approved for moderate to severe psoriasis, but withdrawn as therapy in the United States after several reports of significant hepatotoxicity.
Guselkumab is a human monoclonal IgG1λ antibody that selectively binds to the p19 subunit of interleukin 23 and inhibits its interaction with the IL-23 receptor and is used to treat psoriasis.
Apremilast is a phosphodiesterase 4 (PDE4) inhibitor that blocks production of TNF-α. It is approved as a treatment for active PsA and moderate to severe plaque psoriasis.
Source: Raychaudhuri et al., J Autoimmun 2017
Clinical Pearl: Infliximab is a chimeric human-mouse IgG that binds to tumor necrosis factor alpha (TNF-α) and blocks its activity. TNF-α promotes systemic inflammation and several drugs (including infliximab, adalimumab, etanercept, and apremilast) act to block the effects of TNF-α.
