title: Polarization and apoptosis of T cell subsets in idiopathic thrombocytopenic purpura.
abstract: 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 and apoptosis profiles of T lymphocytes remain unclear completely. In this paper, we investigated the polarization of T cell subsets, the expressions of apoptotic proteins Fas/FasL on T cell subsets and the level of antiapoptotic gene bcl-2 and bax mRNA in the bcl-2 family, then discussed the role of them in ITP pathogenesis. We demonstrated that the ratios of Th1/Th2 and Tc1/Tc2 in ITP children increased obviously, the average percentages of Th1 and Th2 also increased clearly, but the average percentages of Tc1 and Tc2 did not changed. In ITP children, the expressions of Fas, FasL on Th, Th1, Th2, Tc, Tc1 and Tc2 increased significantly. The expressions of FasL on Th1 and Tc1 increased sharply vs. Fas, whereas the expressions of Fas on Th2 and Tc2 increased obviously vs. FasL. The expressions of bcl-2 mRNA in ITP children increased significantly, but the expressions of bax mRNA decreased, the ratios of bcl-2/bax mRNA were improved obviously and there were positive correlation between the ratios of Th1/Th2 (IFN-gamma(+)T/IL-4(+)T) and the ratios of bcl-2/bax mRNA. Taken together, our findings indicate that ITP is Th1 type cell predominant disease although the precise mechanisms await further functional assay. This abnormal polarization of T cell subsets might be related to the high ratios of bcl-2/bax mRNA and the abnormal expressions of Fas, FasL on T cell subsets, as can involve in ITP immunopathogenesis.
authors.affiliation: Department of Transfusion Medicine, Second People's Hospital of Shenzhen City, Affiliated Hospital of Southern Medical University, ShenZhen, China. wuchlin@126.com
authors.forename: W U
authors.initials: WU
authors.lastname: Chang-Lin
authors.forename: X U E
authors.initials: XU
authors.lastname: Jian-Cheng
authors.forename: L I U
authors.initials: LI
authors.lastname: Fang
authors.forename: X I A O
authors.initials: XI
authors.lastname: Hong
authors.forename: Z H U O
authors.initials: ZH
authors.lastname: Xue-Min
authors.forename: C H E N
authors.initials: CH
authors.lastname: Qun
authors.forename: L V
authors.initials: LV
authors.lastname: Xue-Wen
mesh_terms: D017209:Apoptosis / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D053222:Fas Ligand Protein / Q000097:blood; D005260:Female; D006801:Humans; D007223:Infant; D007371:Interferon-gamma / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000276:immunology*; D012333:RNA, Messenger / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis; D019014:fas Receptor / Q000097:blood
chemical_list: C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C508598:IL4 protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D015847:Interleukin-4; D007371:Interferon-gamma