Significance of the imbalance of Th1/Th2 function after acute myocardial infarction
- VernacularTitle:急性心肌梗死后辅助性T细胞功能失衡的意义
- Author:
Xiang CHENG
;
Yuhua LIAO
;
Hongxia GE
;
Bin LI
;
Ying LIU
;
Zhangqiang GUO
;
Ling ZHANG
- Publication Type:Journal Article
- Keywords:
Myocardial infarction;
T-lymphocytes, helper-inducer;
Interferon type Ⅱ;
Interleukin-4;
Ventricular remodeling
- From:
Chinese Journal of Pathophysiology
1999;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: The study explored the significance of the imbalance of Th1/Th2 function after acute myocardial infarction (AMI). METHODS: Peripheral blood mononuclear cells from 33 AMI patients, 22 unstable angina (UA) patients and splenocytes from 35 AMI rats were collected. Cytokine-producing Th cells were monitored by 3-color flow cytometry after stimulated with phorbol myristate acetate (PMA) and ionomycin. IFN-? and IL-4 mRNA in the rat myocardium and chemokine receptors CCR3, CCR5 and CXCR3 mRNA on the surface of rat T lymphocytes after AMI were measured by RT-PCR. RESULTS: Th1 associated cytokine IFN-? significantly increased in patients with AMI and UA within 24 hours after the onset of symptom. the high ratio of IFN-?-producing T cells lasted short in patients with UA and recovered 1 week after the onset. In AMI patients, the high ratio of IFN-?-producing T cells could be examined 1 week and even 1 month after the onset. There was no significant difference on the frequencies of IL-4-producing peripheral T cells between each group. 1 week, 2 weeks and 1 month after AMI, IFN-? mRNA increased in the myocardium of rats, but there was no significant change on cytokine-producing Th cells and chemokine receptors on the surface of rat T lymphocytes. CONCLUSIONS: The Th1/Th2 functional imbalance and up-regulation of Th1 cell-functions exist after AMI and perhaps participate in the onset of AMI. Th1/Th2 functional imbalance may participate in the immune-mediated myocardial injury and ventricular remodeling after AMI as one of the pathogenesises of autoimmune disease.
