Elsohafy Magdy Abdelmageed, Elghzaly Ashraf Antar, Abdelsalam Hebatallah Mansour, Gaballah Mohammad A
Department of Dermatology, Andrology and STDs, Faculty of Medicine, Mansoura University, Egypt.
Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Egypt.
Indian Dermatol Online J. 2019 Jul-Aug;10(4):401-405. doi: 10.4103/idoj.IDOJ_372_18.
Psoriasis is an autoimmune-related chronic inflammatory skin disorder. Psoriasis vulgaris (PV) is the most common form of psoriasis. T regulatory cells (Tregs) are typically considered inhibitors of autoimmune responses. FOXP3 is a master control transcription factor for development and function of Tregs. FOXP3 gene polymorphism changes FOXP3 protein function and quantity leading to Tregs dysfunction that subsequently may be related to PV pathogenesis.
The objective of the present study was to evaluate the possible role of FOXP3 gene (rs3761548) polymorphism in PV pathogenesis.
One hundred sixty subjects were included in the present study (80 PV patients and 80 well-matched healthy controls). All participants were evaluated by detailed history, general examination, dermatological examination, and psoriasis area and severity index (PASI) score. The detection of FOXP3 gene (rs3761548) polymorphism in patients and controls by PCR-restriction fragment length polymorphism technique was done.
There was statistically significant increase in CC genotype and C allele in patients compared to controls, whereas there were non-significant differences in AA and AC genotypes. However, there were non-significant associations between genotype distribution and each of age, sex, family history, PASI score, hair affection, nail affection, hypertension, diabetes mellitus, and body mass index.
FOXP3 gene (rs3761548) polymorphism may increase susceptibility of PV and share in its pathogenesis as it leads to changes in FOXP3 protein function and quantity that subsequently affect T-regs functions. Further investigations for the role of other FOXP3 genes polymorphisms in psoriasis pathogenesis and their effects on the treatment response in psoriasis patients are strongly recommended.
银屑病是一种自身免疫相关的慢性炎症性皮肤病。寻常型银屑病（PV）是银屑病最常见的类型。调节性T细胞（Tregs）通常被认为是自身免疫反应的抑制剂。FOXP3是Tregs发育和功能的主控转录因子。FOXP3基因多态性改变FOXP3蛋白的功能和数量，导致Tregs功能障碍，这随后可能与PV的发病机制有关。
本研究的目的是评估FOXP3基因（rs3761548）多态性在PV发病机制中的可能作用。
本研究纳入160名受试者（80名PV患者和80名匹配良好的健康对照）。所有参与者均通过详细病史、全身检查、皮肤科检查以及银屑病面积和严重程度指数（PASI）评分进行评估。采用聚合酶链反应-限制性片段长度多态性技术检测患者和对照中FOXP3基因（rs3761548）的多态性。
与对照组相比，患者的CC基因型和C等位基因有统计学意义的增加，而AA和AC基因型无显著差异。然而，基因型分布与年龄、性别、家族史、PASI评分、毛发受累、指甲受累、高血压、糖尿病和体重指数之间均无显著关联。
FOXP3基因（rs3761548）多态性可能增加PV的易感性并参与其发病机制，因为它导致FOXP3蛋白功能和数量的变化，进而影响Tregs功能。强烈建议进一步研究其他FOXP3基因多态性在银屑病发病机制中的作用及其对银屑病患者治疗反应的影响。
