Psoriasis vulgaris is a chronic immune-mediated dermatological condition, resulting from an interaction between environmental triggers and genetic susceptibilities. Alteration in the production of the inflammatory mediators plays a pivotal part in the pathogenesis of the disease. Genes encoding the mediators of these inflammatory pathways can dictate susceptibility to psoriasis. These genes have a wide range of functions that involve innate immunity (IFIH1, TRAF3IP2, CARD14, c-REL, DDX58), antigen presentation (HLA-Cw6), T-cells development, maturation, and polarization (RUNX1, RUNX3, STAT3), cytokine signaling (IL12Bp40, IL23Ap19, IL23R, JAK2), and immune regulators (TNIP1, TNFAIP3, IL36RN, SOCS1, ZC3H12C, NFKBIA). The risk alleles of these genes can contribute to the overall state of susceptibility to psoriasis by lowering the threshold of the innate immune response that can eventually provoke the pathogenic adaptive immune responses capable of inducing psoriasis. The investigations on genetic associations of psoriasis may allow the discovery of new diseases modifying targets and possibly open a path for the advancement of personalized medicine. They also allow us to discover new aspects of human skin biology.
Keywords: GWAS; Gene; Immune response; Immunogenetics; Psoriasis; Susceptibility.
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