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目的:探讨抗L3T4单克隆抗体对BALB/c小鼠实验性自身免疫性心肌病的治疗作用及T细胞信号转导机制。方法:以ADP/ATP载体肽免疫小鼠建立自身免疫性心肌病模型。3个月后,向小鼠体内注入抗L3T4单抗,以清除CD4+T细胞,并以无关抗体为对照。通过实时荧光定量PCR检测小鼠T细胞中信号分子(p56lck、p59fyn和Zap-70)和细胞因子(IFN-γ、IL-2和IL-4)的表达;通过免疫组化技术分析各组小鼠T细胞内CD45的表达。结果:给予抗L3T4单抗治疗的DCM小鼠T细胞内信号分子(p56lck、p59fyn和Zap-70)和细胞因子(IFN-γ、IL-2和IL-4)表达均减少,CD45的表达也明显减少。相反,以无关抗体免疫小鼠并不能对其产生保护作用,T细胞信号分子、CD45和细胞因子的表达也不被抑制。结论:抗L3T4单抗可以抑制ADP/ATP载体肽诱导的小鼠DCM过程中的T细胞信号分子和细胞因子的表达,可能起到治疗作用。
Objective: To investigate the therapeutic effect of anti-L3T4 monoclonal antibody on experimental autoimmune cardiomyopathy in BALB / c mice and the mechanism of T cell signal transduction. Methods: The model of autoimmune cardiomyopathy was established by immunizing mice with ADP / ATP carrier peptide. Three months later, mice were injected with anti-L3T4 mAb to clear CD4 + T cells and used as an irrelevant antibody. The expression of signal molecules (p56lck, p59fyn and Zap-70) and cytokines (IFN-γ, IL-2 and IL-4) in mouse T cells were detected by real-time fluorescence quantitative PCR. CD45 expression in murine T cells. Results: The expression of the signal molecules (p56lck, p59fyn and Zap-70) and cytokines (IFN-γ, IL-2 and IL-4) in T lymphocytes of mice treated with anti-L3T4 mAb decreased, obviously decrease. In contrast, immunization of mice with irrelevant antibodies did not protect them, nor was the expression of T-cell signaling molecules, CD45 and cytokines. CONCLUSION: The anti-L3T4 mAb may inhibit the expression of T-cell signal molecules and cytokines in ADP / ATP carrier peptide-induced mouse DCM and may play a therapeutic role.