T-bet、GATA-3、FoxP3及CD_4^+CD_(25)^+调节性T细胞在AA发病机制中的作用  

The role of transcription factor T-bet,GATA-3,FoxP3 and CD_4^+CD_(25)^+ regulatory T cells in patients with aplastic anemia

作　　者：沈红石[1] 陈海飞[1] 任传路[1] 李征洋[1] 唐杰庆[1] 王静[1] 吴天勤[1] 

机构地区：[1]中国人民解放军第100医院,江苏苏州215007

出　　处：《山东医药》2013年第4期8-10,13,共4页Shandong Medical Journal

基　　金：全军医药卫生科研项目(07MA018;08MA019)

摘　　要：目的探讨转录因子T-bet、GATA-3和CD+4CD+25调节性T细胞及其转录因子FoxP3在再生障碍性贫血(AA)发病机制中的作用。方法选择AA患者27例(AA组)、体检健康者25例(对照组),采用RT-PCR技术检测两组外周血单个核细胞(PBMCs)中Th1、Th2细胞及CD4+CD2+5调节性T细胞特异性转录因子T-bet、GATA-3、FoxP3 mR-NA的表达,运用流式细胞术检测外周血中T淋巴细胞亚群,ELISA法检测血浆中Th1和Th2类细胞因子IFN-γ、IL-4水平。结果与对照组相比,AA组的血浆T-bet mRNA相对表达量升高(P<0.01),GATA-3与FoxP3 mRNA相对表达量降低(P<0.05,P<0.01);AA组外周血中CD+3、CD+3CD+8T细胞占淋巴细胞的百分比较对照组升高(P均<0.05),CD+3CD+4、CD+4CD+25T细胞占淋巴细胞的百分比和CD+4/CD+8值较对照组降低(P<0.05或P<0.01);AA组血浆中IFN-γ水平及IFN-γ/IL-4高于对照组(P均<0.01)。结论 AA患者存在CD+4CD+25调节性T细胞及其特异性转录因子FoxP3 mRNA表达下调,调节性T细胞的减少及由此引起免疫抑制效应不足可能是AA发生的重要原因之一。Objective To probe into the role of transcription factors T-bet,GATA-3 in the pathogenesis of aplastic a- nemia, and the relationship between CD4^＋CD25^＋ regulatory T ceils, transcription factor FoxP3 and the development of aplastic anemia. Methods A total of 27 patients with AA and 25 healthy people （ control group ） were selected. The expression of T-bet, GATA-3 and FoxP3 mRNA were detected by Real Time PCR. The expression of T lymphocyte subsets were detected by flow cytometi＇y on peripheral blood mononuclear cell IFN-γ and IL-4 were determined by ELISA. Results Compared with the control group, the expression of T-bet mRNA in the AA group significantly increased （P 〈 0.01 ）, while the ex- pression of GATA-3 and FoxP3 mRNA decreased （ P 〈 0. 05 or P 〈 0. 01 ）. The expression of T lymphocyte subsets of CD3^＋, CD3^＋ CD8^＋ T percentage increased （ P 〈 0. 05）, while CD3^＋ CD4^＋, CD4^＋ CD25^＋ and the ratio of CD4^＋ and CD8^＋ decreased （P 〈 0.05 or P 〈 0. 01 ）. And the level of IFN-γand IFN--//IL-4 in the AA group were significantly higher than those in con- trol group （P 〈0.01 ）. Conclusions There is functional disorder of T lymphocyte subsets and activation of B lymphocyte proliferation at aplastic anemia. The expression of CD4^＋CD25^＋ regulatory T ceils is reduced, and its special transcription fac- tor FoxP3 mRNA is decreased, which indicated that insufficient immunosuppressive effects resulting from the reduction of regulatory T cells may be one important reason the immune imbalance of aplastie anemia.

关 键 词：T-BET基因 GATA-3基因 FOXP3基因 转录因子 干扰素γ 白细胞介素4 CD+4CD+25调节性T细胞 再生障碍性贫血 

分 类 号：R392.11[医药卫生—免疫学]