摘要
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。
AIM： We examined the efficacy of anti - L3T4 McAb in the T cell signaling pathway in treating experimental autoimmune cardiomyopathy in BALB/c mice, as a model of the autoimmune mechanism involved in human dilated cardiomyopathy （DCM）. METHODS： ADP/ATP cartier peptides were used to induce autoimmune cardiomyopathy in BALB/c mice. After 3 months, anti - L3T4 McAb was administered to deplete CD4^＋ T cells in the mice. Real - time PCR were used to detect the expression of intracellular signaling molecules （p561ck, p59fyn and Zap -70） and cytokine production （IFN -γ, IL -2 and IL -4） in T cells. The expression of CD45 was determined by immunohistochemistry analysis. RESULTS ： Reduced expression of p561ck, p59fyn and Zap - 70 and the reduced cytokine production of IFN - γ, IL - 2 and IL - 4 in T cells of anti - L3T4 - treated DCM mice were found. Also, the expression of CD45 in spleen T cells was significantly decreased in the anti -L3T4 -treated group. In contrast, immunization with irrelevant Ab did not protect the mice, the expression of T cell signaling molecules, CD45, and cytokine were not inhibited. CONCLUSION： These studies provide direct evidence that anti - L3T4 McAb can be an effective immunomodulator to T cell signal molecules and subsequent cytokine production events in ADP/ATP cartier - induced DCM in BALB/c mice.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2008年第9期1676-1681,共6页
Chinese Journal of Pathophysiology
基金
National Natural Science Foundation of China(No.30000070)
关键词
T淋巴细胞
CD4
单克隆抗体
信号转导
心肌病
T - lymphocytes
CD4
Monoclonal antibody
Signal transduction
Cardiomyopathy
