Babaie Farhad, Omraninava Melodi, Gorabi Armita Mahdavi, Khosrojerdi Arezou, Aslani Saeed, Yazdchi Arsalan, Torkamandi Shahram, Mikaeili Haleh, Sathyapalan Thozhukat, Sahebkar Amirhossein
Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Department of Medical Genetics and Immunology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Curr Genomics. 2022 Jul 5;23(3):163-174. doi: 10.2174/1389202923666220527111037.
Psoriasis is an organ-specific autoimmune disease characterized by the aberrant proliferation and differentiation of keratinocytes, leading to skin lesions. Abnormal immune responses mediated by T cells and dendritic cells and increased production of inflammatory cytokines have been suggested as underlying mechanisms in the pathogenesis of psoriasis. Emerging evidence suggests that there is a heritable basis for psoriatic disorders. Moreover, numerous gene variations have been associated with the disease risk, particularly those in innate and adaptive immune responses and antigen presentation pathways. Herein, this article discusses the genetic implications of psoriatic diseases' etiopathogenesis to develop novel investigative and management options.
银屑病是一种器官特异性自身免疫性疾病，其特征为角质形成细胞异常增殖和分化，导致皮肤病变。T细胞和树突状细胞介导的异常免疫反应以及炎症细胞因子产生增加被认为是银屑病发病机制的潜在机制。新出现的证据表明，银屑病相关疾病存在遗传基础。此外，众多基因变异与疾病风险相关，尤其是那些参与固有免疫和适应性免疫反应以及抗原呈递途径的基因变异。本文将探讨银屑病病因发病机制的遗传学意义，以开发新的研究和管理方案。
