Abstract
Psoriasis is a complex chronic inflammatory cutaneous disorder. To date, robust molecular mechanisms of psoriasis have been reported. Among diverse aberrant immunopathogenetic mechanisms, the current model emphasizes the role of Th1 and the IL-23/Th17 axis, skin-resident immune cells and major signal transduction pathways involved in psoriasis. The multiple genetic risk loci for psoriasis have been rapidly revealed with the advent of a novel technology. Moreover, identifying epigenetic modifications could bridge the gap between genetic and environmental risk factors in psoriasis. This review will provide a better understanding of the pathogenesis of psoriasis by unraveling the complicated interplay among immunological abnormalities, genetic risk foci, epigenetic modification and environmental factors of psoriasis. With advances in molecular biology, diverse new targets are under investigation to manage psoriasis. The recent advances in treatment modalities for psoriasis based on targeted molecules are also discussed.
Highlights
Psoriasis is a chronic relapsing cutaneous inflammatory disorder
A mouse model in which symptomless psoriatic skin was engrafted in severely immunodeficient mice lacking functional natural killer (NK) cells, T cells or B cells revealed the spontaneous production of psoriatic skin lesions, suggesting that tissue-resident immune cells themselves can be a major source for the development of psoriasis [54]
The susceptibility loci for psoriasis contain many genes associated with disease pathogenesis such as genes involved in antigen presentation, Th1 cell differentiation, Th17 cell differentiation, nuclear factor κB (NF-κB) signaling, IFN signaling and keratinocyte proliferation
Summary
Psoriasis is a chronic relapsing cutaneous inflammatory disorder. The skin lesion of psoriasis is classically characterized by erythematous papules and plaques with white thick scales. Different clinical phenotypes of the disease can be observed even in the same patients in the course of the disease progression. The prevalence rate of psoriasis varies in different populations, ranging from 0.91–8.5% [2]. Enamandram et al [3] surmised that the reason for such diverse prevalence rates of psoriasis among different populations might be associated with genetic susceptibility and environmental factors. Since the clinical characteristic of psoriasis is manifested as thick scales with the histopathological characteristic of epidermal hyperplasia, psoriasis has been regarded as a disorder of keratinocytes. Recent progress in molecular mechanisms of psoriasis that contribute to the initiation and development of psoriasis will be described, especially in the field of immunologic abnormalities, signaling pathways, genetics and epigenetics.
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