Polarization and Apoptosis of T Cell Subsets in Idiopathic Thrombocytopenic Purpura

作     者：Fang Liu~(1,2) Changlin WU~1 Xiaomeng Yang~1 Hong Xiao~1 Xuemin Zhuo~1 Zhengwei Cheng~1 Qun Chen~1 ~1Department of Microbiology and Immunology,Guangdong Medical College,Zhanjiang,Guangdong 524023,China ~2Department of Microbiology and Immunology,Guangdong Medical College,No.2 Wen-ming East Road,Zhanjiang,Guangdong 524023,China. 

作者机构：Department of Microbiology and Immunology Guangdong Medical College Zhanjiang China. liufang@*** 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2005年第2卷第5期

页      面：387-392页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：supported by Guangdong Natural Science Foundation(Society Development Domain No.2004024) 

主　　题：idiopathic thrombocytopenic purpura polarization apoptosis T cell subset 

摘      要：It is well-known that idiopathic thrombocytopenic purpura （ITP） is an acquired organ-specific autoimmune hemorrhagic disease and dysfunctional cellular immunity is considered important in the pathophysiology of ITP. However, polarization patterns and apoptosis profiles of T lymphocytes remain unclear. In this study, we investigated the polarization of T cell subsets, the expressions of apoptotic proteins Fas/FasL on the subsets and the level of anti-apoptotic gene bcl-2 and bax mRNA. It was demonstrated that the ratios of Thl/Th2 and Tcl/Tc2 in ITP children were increased obviously and that the average percentages were increased clearly for Thl and Th2, but not for Tcl and Tc2. In ITP children, the enhancing expressions were detected for FasL on Thl and Tcl and for Fas on Th2 and Tc2. With increasing level of bcl-2 mRNA and decreasing expression of bax mRNA in ITP children, the ratio of bcl-2/bax mRNA was improved obviously, which was positive correlated with the ratio of Thl/Th2. Taken together, our findings indicate that ITP is a Thl predominant disease. This polarization pattern of T cell subsets might be related to the high ratio of bcl-2/bax mRNA and the abnormal expressions of Fas and FasL on T cell subsets.