Newer research has suggested the involvement of interconnected factors for the heterogeneous presentation of psoriatic disease. Psoriasis and psoriatic arthritis are evolved by the triggers from a mixture of genetic risk loci, most of which are involved in the regulation of IL-23 receptor signaling and the NF-kB pathway, inequalities in Treg/T17 immunity, and alterations in the gut and cutaneous microbiome. 

These genetic variants and the interactions taking place in a microenvironment among immune cells, KCs, osteoclasts, and the microbiome define the development of psoriatic disease, disease severity, therapeutic response, and the development of co-morbidities like inflammatory arthritis and cardiometabolic conditions. 

These explanations of the pathophysiology have exposed novel therapeutic targets and have also provided data to optimize treatment for the individual patient. Implementing these in the clinical setting will help deliver more timely, effective, and personalized care.

Source: Yan D, Gudjonsson JE, Le S, Maverakis E, Plazyo O, Ritchlin C, Scher JU, Singh R, Ward NL, Bell S, Liao W. New Frontiers in Psoriatic Disease Research, Part I: Genetics, Environmental Triggers, Immunology, Pathophysiology, and Precision Medicine, JID, 2021; 141(9):2112-2122. DOI:https://doi.org/10.1016/j.jid.2021.02.764