Abstract
Psoriasis is an erythematous-squamous dermatosis with a polygenic inheritance history. Both environmental and genetic factors play a role in the etiology of the disease. Over the past two decades, numerous linkage analyzes and genome-wide association studies have been conducted to investigate the role of genetic variation in disease pathogenesis and progression. To date, >70 psoriasis susceptibility loci have been identified, including HLA-Cw6, IL12B, IL23R, and LCE3B/3C. Some genetic markers are used in clinical diagnosis, prognosis, treatment, and personalized new drug development that can further explain the pathogenesis of psoriasis. This review summarizes the immunological mechanisms involved in the etiopathogenesis of psoriasis and recent advances in susceptibility genes and highlights new potential targets for therapeutic intervention.
Highlights
Psoriasis is a clinically common chronic inflammatory disease characterized by skin tissue damage and concomitant other systemic complications.[1,2] psoriasis is more common in American, Canadian, and European populations, it is seen all over the world affecting $1 to 3% of the world’s population.[3]
This review summarizes the immunological mechanisms involved in the etiopathogenesis of psoriasis and recent advances in susceptibility genes and highlights new potential targets for therapeutic intervention
We summarize what is currently known about the immunogenetics of psoriasis pathogenesis
Summary
Psoriasis is a clinically common chronic inflammatory disease characterized by skin tissue damage and concomitant other systemic complications.[1,2] psoriasis is more common in American, Canadian, and European populations, it is seen all over the world affecting $1 to 3% of the world’s population.[3] This disease usually presents with clinical and histological features such as adherent, raised silver scales, dividing lines, and oval-shaped plaques with erythema.[4] Psoriasis is considered to occur through chronic interactions between hyperproliferative keratinocytes and activated immune cells. Cellular and molecular contributions have been demonstrated in response to an overactive immune response.[5] Since psoriasis is a skin-specific autoimmune disease, cytokines, chemokines, adhesion factors, epidermal growth factors, nerve growth factors, and especially Th1 and Th17 polarization play a role in its pathogenesis (►Fig. 1).[6] the exact cause of psoriasis is unknown, its genetics are complex and multifactorial. We summarize what is currently known about the immunogenetics of psoriasis pathogenesis
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