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目的:通过研究T细胞信号分子的表达,探讨自身免疫性扩张型心肌病发生的分子机制。方法:以线粒体腺苷酸转位酶(ANT)合成肽免疫液免疫Balb/c小鼠,建立自身免疫性扩张型心肌病动物模型(DCM组),运用实时荧光定量PCR法检测其T细胞内P56lck的表达,流式细胞术检测其Th细胞内IFN-γ和IL-4的含量,ELISA法检测其血清抗ANT自身抗体水平,免疫组化法观察其T细胞表面CD45的表达。以不含ANT合成肽免疫液免疫小鼠作为对照组(control),试验期6个月。结果:DCM组小鼠P56lck的基因表达(1369·51±874·05vs47·93±10·21,P<0·01)、IFN-γ和IL-4的百分含量(尤其是IL-4)(8·27±1·29vs5·58±0·59,P<0·01;9·93±1·53vs2·05±0·21,P<0·01)、抗ANT自身抗体的水平(0·105±0·015vs0·006±0·002,P<0·01)、CD45的表达强度(0·154±0·021vs0·026±0·008,P<0·01)均明显高于对照组。结论:异常的T细胞受体信号转导通路在ANT肽诱导扩张型心肌病发生中起着重要作用。
Objective: To investigate the molecular mechanism of autoimmune dilated cardiomyopathy by studying the expression of T cell signaling molecules. Methods: Balb / c mice were immunized with synthetic immunostimulating peptide of mitochondrial adenylate translocase (ANT) to establish an autoimmune dilated cardiomyopathy model group (DCM group). The expression of T cell was detected by real-time fluorescence quantitative PCR P56lck was detected by flow cytometry. The levels of IFN-γ and IL-4 in Th cells were detected by flow cytometry. The level of serum anti-ANT autoantibodies was detected by ELISA. The expression of CD45 on T cells was detected by immunohistochemistry. The mice were immunized with ANT-free synthetic immunization solution for 6 months. Results: The gene expression of P56lck in DCM group (1369.51 ± 874.05 vs 47.93 ± 10.21, P <0.01), the percentage of IFN-γ and IL-4 (especially IL-4) (8 · 27 ± 1 · 29vs5 · 58 ± 0 · 59, P <0.01 · 9 · 93 ± 1 · 53vs2 · 05 ± 0 · 21, P <0.01) and the levels of anti-ANT autoantibodies · 105 ± 0 · 015vs0 · 006 ± 0 · 002, P <0.01), CD45 expression intensity (0 · 154 ± 0 · 021vs0 · 026 ± 0 · 008, P <0.01) were significantly higher than the control group. Conclusion: Abnormal T cell receptor signal transduction pathway plays an important role in the development of dilated cardiomyopathy induced by ANT peptide.