摘要
目的:通过研究急性丙型肝炎病毒(HCV)感染患者外周血中FOXP3的表达,初步探讨其在急性丙型肝炎发病机制中的临床意义。方法:选择急性丙型肝炎患者与健康人各21例,用流式细胞仪检测外周血CD4+CD25+T细胞的数量;ELISA试剂盒检测患者和正常对照组外周血培养上清中Th2型细胞因子(IL-10)和Th1型细胞因子(IL-2)的表达;RT-PCR检测FOXP3的mRNA表达。结果:在急性HCV患者外周血中CD4+CD25+T细胞约占CD4+T细胞(28.2±2.1)%,显著高于正常人外周血中CD4+CD25+T细胞(2.7±0.7)%(P=0.032);急性HCV组外周血CD4+CD25+T细胞高表达FOXP3;急性HCV组外周血单个核细胞(PBMC)培养上清主要分泌IL-10,而IL-2分泌无显著变化。结论:急性HCV感染者Th1免疫抑制可能与外周血CD4+CD25+T细胞高表达FOXP3有关。
Objective:To study the role of FOXP3 in patients with acute infection of hepatitis C virus. Methods:Flow cytometry was used to determine the number of CD4+CD25+T cells in peripheral blood;the levels of the Th1 / Th2 cytokines secretion of PBMC in patients and healthy donors were detected by ELISA;the expression of FOXP3 mRNA was measured by RT-PCR. Results:CD4+CD25+ T cells comprised (28.2±2.1)% of peripheral CD4+T cells in the blood of acute hepatitis C virus infected patients,and it was significantly higher than that of healthy controls(2.7±0.7)%(P=0.032). CD4+CD25+T cells in the peripheral blood of acute hepatitis C virus infected patients highly expressed FOXP3. Compared with the cytokines levels of normal control,the levels of IL-10 was notably increased (P 〈 0.01) while IL-2 was not detected in the culture supernatant of PBMCs from patients. Conclusion:Patients with acute hepatitis C virus infection showed an increased number of FOXP3,which suppressed Th1 response.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2010年第2期242-244,共3页
Journal of Nanjing Medical University(Natural Sciences)