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慢性丙型肝炎自身免疫发病机制的研究
引用本文:刘文恩,谭德明,张铮.慢性丙型肝炎自身免疫发病机制的研究[J].中南大学学报(医学版),2000,25(4):367-370.
作者姓名:刘文恩  谭德明  张铮
作者单位: 
基金项目:霍英东青年基金!资助 ( 93 0 65 )
摘    要:为探讨慢性丙型肝炎自身免疫的发病机制 ,用免疫学方法检测慢性HCV感染者、慢性HBV感染者和健康献血员的血清抗GOR ,ANA和TGA/TMA ,另检测部分慢性HCV感染者和健康献血员血清可溶性Fas(sFas)水平 ;用间接免疫荧光和流式细胞术检测部分慢性HCV感染者和健康献血员外周血淋巴细胞亚群及其凋亡百分率。结果显示 :慢性HCV感染者抗GOR ,ANA和TGA/TMA的阳性率及血清sFas浓度较正常对照组显著增高 (均为 P >0 .0 1) ,较慢性HBV感染者的抗GOR和ANA阳性率亦显著增高 (P <0 .0 1和P <0 .0 5 ) ;慢性HCV感染者PBMCs及CD+ 3 T淋巴细胞凋亡明显高于正常对照组 (P <0 .0 5 ) ,其抗GOR阳性者CD+ 4T淋巴细胞及CD+ 19B淋巴细胞凋亡比抗GOR阴性者明显减少 (P <0 .0 1和P <0 .0 5 )。表明 :慢性HCV感染者存在自身免疫反应及淋巴细胞凋亡不均衡现象 ;CD+ 4T细胞及CD+ 19B细胞凋亡的减少在慢性HCV感染诱导的自身免疫反应中起重要作用。血清sFas水平升高可能是部分淋巴细胞凋亡减少 ,导致自身免疫的原因之一。

关 键 词:丙型肝炎病毒    丙型肝炎    自身免疫    脱噬作用    病理生理学    
修稿时间:1999-09-05

A study of the autoimmune pathogenesis of chronic HCV infection
LIU Wen en,TAN De ming,ZHANG Zheng,et al.A study of the autoimmune pathogenesis of chronic HCV infection[J].Journal of Central South University (Medical Sciences)Journal of Central South University (Medical Sciences),2000,25(4):367-370.
Authors:LIU Wen en  TAN De ming  ZHANG Zheng  
Institution:Department of Infectious Diseases, Xiangya Hospital, Hunan Medical University(Changsha 410008) [
Abstract:To explore the autoimmune pathogenesis of chronic hepatitis C virus(HCV) infection. Anti GOR, antinuclear anbitobides(ANA), thyroglobulin antibody(TGA), thyroid microsome antibody(TMA), serum levels of soluble Fas(sFas), and peripheral blood lymphocyte(PBMC) subsets and their apoptosis were measured in chronic HCV infection by using immunity assay and flow cytometry, respectively. The results showed that the positive rates of anti GOR, ANA and TMA/TGA were significantly higher in chronic HCV infected patients than those in normal controls(P<0.01, respectively). In comparison with chronic HBV infected patients, anti GOR and ANA were also significantly increased in chronic HCV infected patients(P<0.01, P<0.05, respectively). The serum levels of sFas were significatly higher in chronic HCV infection than those in healthy donors(P<0.01). The apoptosis percentage of PBMCs and CD + 3 cell was all increased in chronic HCV infection(vs normal controls P<0.05). However, the apoptosis percentages of CD + 4 T and CD + 19 B cells in PBMCs were significantly decreased in patients with anti GOR positive as compared with anti GOR negative(P<0.01, P<0.05). The results indicate that autoimmune reactions and the imbalance of lymphocyte apoptosis exist during chronic HCV infection. Decreasing of the apoptosis of CD + 4 T and CD + 19 B lymphocytes may be the important reasons for the mechanism of autoimmune pathogenesis of chronic HCV infection. Increased serum levels of sFas may be responsible for the decrease of the apoptosis in a part of lymphocytes in chronic HCV infection.
Keywords:hepatitis C virus  hepatitis C  autoimmunity  apoptosis  pathophysiology
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