Moorchung Nikhil N, Vasudevan Biju, Chatterjee Manas, Grewal Rajan Singh, Mani Narayana S
Department of Pathology, Armed Forces Medical College and Command Hospital, Pune, Maharashtra, India.
Department of Dermatology, Armed Forces Medical College and Command Hospital, Pune, Maharashtra, India.
Indian J Dermatol. 2015 Jul-Aug;60(4):345-50. doi: 10.4103/0019-5154.160477.
Tumor necrosis factor-alpha (TNFα) is an important inflammatory mediator in psoriasis and several genetic polymorphisms of this cytokine have been reported. Majority of studies have focused on the increased G- A polymorphism at the -308 position in psoriasis. There has been no comprehensive study evaluating the genetic polymorphisms, TNFα expression in the skin and histopathology. We are undertaking this study to outline TNFα genetic polymorphisms, its skin expression and histopathological correlation to help determine its role at the genetic and protein level.
112 patients of psoriasis and 243 healthy controls were included in this prospective study. 5 ml of peripheral blood was collected to study the TNFα genetic polymorphisms by polymerase chain reaction and restriction fragment length polymorphism analysis. Histopathological analysis of biopsies from the 112 patients were done using visual analogue scale and correlated with the findings. 61 of these cases were analyzed for TNFα expression by immunohistochemistry. The results of study were statistically analyzed using SPSS 13.0 statistical package program.
A strong association of TNFα -308 G/A polymorphism in psoriasis cases was detected. The A allele of the TNFα -308 G/A polymorphism occurs rarely in the Indian population, however there is an over representation of this allele in psoriatic patients. There was no association seen between TNFα genotype and histopathological severity of psoriasis.
The study emphasized the central role of TNFα in the pathogenesis of psoriasis. TNFα genotyping may be helpful in identifying subjects in whom anti-TNFα therapeutic strategies may be tried.
肿瘤坏死因子-α（TNFα）是银屑病中的一种重要炎症介质，并且已经报道了该细胞因子的几种基因多态性。大多数研究集中在银屑病中-308位点的G-A多态性增加。尚未有全面的研究评估基因多态性、皮肤中TNFα的表达以及组织病理学。我们正在进行这项研究，以概述TNFα基因多态性、其皮肤表达以及组织病理学相关性，以帮助确定其在基因和蛋白质水平上的作用。
本前瞻性研究纳入了112例银屑病患者和243例健康对照。采集5毫升外周血，通过聚合酶链反应和限制性片段长度多态性分析研究TNFα基因多态性。对112例患者的活检组织进行组织病理学分析，使用视觉模拟评分法并与研究结果相关联。其中61例通过免疫组织化学分析TNFα表达。使用SPSS 13.0统计软件包程序对研究结果进行统计学分析。
在银屑病病例中检测到TNFα -308 G/A多态性存在强关联。TNFα -308 G/A多态性的A等位基因在印度人群中很少出现，然而在银屑病患者中该等位基因的比例过高。未发现TNFα基因型与银屑病组织病理学严重程度之间存在关联。
该研究强调了TNFα在银屑病发病机制中的核心作用。TNFα基因分型可能有助于识别可尝试抗TNFα治疗策略的受试者。
