目的：检测斑块型银屑病患者外周血单个核细胞（PMBCs ）中p16基因启动子甲基化的状态，探讨p16基因甲基化的检测在斑块型银屑病发病中的作用和机制。方法收集2011年4月至2012年5月该院门诊和住院48例斑块型银屑病患者（实验组）和18例健康者（对照组）的外周血单个核细胞（PBMCs），采用甲基化特异性聚合酶链反应（MSP）检测PBMCs中p16基因甲基化的状态，并分析p16基因甲基化与患者病程和银屑病皮损面积和严重程度指数（PASI）评分的关系。结果斑块型银屑病患者PBMCs中p16基因甲基化状态（31．3％）明显高于对照组（5．6％），差异具有统计学意义（χ2＝4．71，P＜0．05），且与PASI评分之间差异具有统计学意义（t＝2．63， P＜0．05），而与患病病程之间差异无统计学意义（t＝0．55，P＞0．05）。结论斑块状银屑病患者PBMCs中p16基因呈高甲基化比例明显增高状态，可能参与斑块状银屑病的发病机制。%Objective To detect the methylation of p16 gene promoter in peripheral blood mononuclear cell (PMBCs) in patients with plaque psoriasis and to research its function and mechanism in the pathogenesis of plaque psoriasis .Methods From 2011 .4 to 2012 .5 collected and tested the PBMCs from 48 plaque psoriasis patients (ex-periment group) and 18 healthy controls (control group) ,and detected the methylation of p16 gene promoted in PB-MCs with methylation specific PCR (MSP) ,and analyzed the relationship between p16 gene methylation and course of disease and PASI credits .Results The rates of p16 gene methylation (31 .3% ) in psoriatic patients was higher compared with the controls (5 .6% ) (χ2 =4 .71 ,P<0 .05) and demonstrated significant difference and significantly coincident with PASI (t=2 .63 ,P<0 .05) ,but there was no significant difference compared with course of disease (t=0 .55 ,P>0 .05) .Conclusion The rates of p16 gene methylation in PBMCs in plaque psoriasis patients was sig-nificantly higher than the controls ,and it suggests that the hyper-methylation of p16 gene may play an important role in the pathogenesis of plaque psoriasis .
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