Molecular and cellular regulation of psoriatic inflammation

Abstract

This review highlights the molecular and cellular mechanisms underlying psoriatic inflammation with an emphasis on recent developments which may impact on treatment approaches for this chronic disease. We consider both the skin and the musculoskeletal compartment and how different manifestations of psoriatic inflammation are linked. This review brings a focus to the importance of inflammatory feedback loops that exist in the initiation and chronic stages of the condition, and how close interaction between the epidermis and both innate and adaptive immune compartments drives psoriatic inflammation. Furthermore, we highlight work done on biomarkers to predict the outcome of therapy as well as the transition from psoriasis to psoriatic arthritis.

Risk of Candida Infection and Serious Infections in Patients with Moderate-to-Severe Psoriasis Receiving Biologics: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

“…Psoriasis is a common, easy-to-relapse, chronic inflammatory skin disorder, affecting approximately 2% of the general population, with significant morbidity and a long course [1,2]. Most patients with psoriasis suffer from chronic plaque psoriasis, which accounts for 80%-90% of all cases [3]. Psoriasis is not only manifested by cutaneous symptoms but also associated with a high risk of other diseases [4], such as psoriatic arthritis, cardiovascular disease, insulin resistance, and mental health disorders, thus causing a severe burden to patients and society [5].…”

“…Psoriasis was originally thought as a keratinocyte-driven autoinflammatory condition given the dysfunctional proliferation of keratinocytes. Nevertheless, research conducted in the 1970s identified a significant role for T cells, emphasizing their role in autoimmunity [3]. e interleukin (IL)-17/tumor necrosis factor-α (TNFα)/IL-23 axis is currently considered to be crucial in the pathogenesis of psoriasis [6].…”