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Role of activation-induced cell death in pathogenesis of patients with chronic hepatitis B

机译:活化诱导的细胞死亡在慢性乙型肝炎患者发病机制中的作用

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AIM: To study and compare the difference of activation-induced cell death (AICD) in peripheral blood T-lymphocytes (PBL-Ts) from patients with chronic hepatitis B (CHB) and the normal people in vitro, and to explore the role of AICD in chronic hepatitis B virus (HBV) infection and the pathogenesis of CHB. METHODS: Twenty-five patients and fourteen healthy people were selected for isolation of PBL-Ts. During cultivation, anti-CD3 mAb, PMA and ionomycin were used for AICD of PBL-Ts. AICD ratio of PBL-Ts was detected with TdT-mediated dUTP nick end labeling and assessed by flow cytometry. RESULTS: When induced with anti-CD3, PMA and ionomycin in vitro, AICD ratio of PBL-Ts from CHB patients was significantly higher than that from healthy control (17.24+-1.21 vs. 6.63+-1.00, P<0.01) and that from CHB patients without induction (17.24+-1.21 vs. 9.88+-1.36, P<0.01). There was a similar AICD ratio of PBL-Ts between induction group and without induction group, but no difference was found before and after induction in healthy control. The density of INF-γ in culture media of induction groups of CHB was lower than that of other groups (P<0.01). There was no difference between these groups in density of IL-10 (P<0.05). CONCLUSION: When induced during cultivation in vitro, PBL-Ts from CHB have AICD very commonly. This phenomenon has a potentially important relation with pathogenesis of CHB and chronicity of HBV infection.
机译:目的:研究和比较慢性乙型肝炎(CHB)患者和正常人外周血T淋巴细胞(PBL-Ts)中活化诱导细胞死亡(AICD)的差异,并探讨其作用。 AICD在慢性乙型肝炎病毒(HBV)感染和CHB的发病机理中。方法:选择25例患者和14例健康人进行PBL-Ts分离。培养期间,抗CD3 mAb,PMA和离子霉素用于PBL-Ts的AICD。用TdT介导的dUTP缺口末端标记检测PBL-Ts的AICD比,并通过流式细胞术评估。结果:在体外用抗CD3,PMA和离子霉素诱导时,CHB患者的PBL-Ts AICD比明显高于健康对照组(17.24 + -1.21 vs. 6.63 + -1.00,P <0.01),且来自没有诱导的CHB患者(17.24 + -1.21对9.88 + -1.36,P <0.01)。诱导组和非诱导组之间PBL-Ts的AICD比值相似,但健康对照组在诱导前后均无差异。 CHB诱导组的培养基中INF-γ的浓度低于其他各组(P <0.01)。这些组之间的IL-10密度无差异(P <0.05)。结论:在体外培养过程中,CHB的PBL-Ts具有AICD。这种现象与CHB的发病机理和HBV感染的慢性具有潜在的重要关系。

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