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Molecular Mechanisms and Management of a Cutaneous Inflammatory Disorder: Psoriasis

Journal

Publisher

MDPI
DOI: 10.3390/ijms18122684

Keywords

biologics; epigenetics; genetics; interleukin-23; psoriasis; signaling pathway; small molecules; T helper 17 cells

Funding

  1. Basic Science Research program and Creative Materials Discovery Program through the National Research Foundation of Korea (NRF)
  2. Ministry of Education, Science and Technology and the Ministry of Science, ICT and Future Planning [2015R1C1A2A01055073, 2016M3D1A1021387]
  3. National Research Foundation of Korea [2015R1C1A2A01055073, 2016M3D1A1021387] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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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.

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