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Significance of the imbalance of Th1/Th2 function after acute myocardial infarction / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1999.
Artigo em Chinês | WPRIM | ID: wpr-525790
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.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 1999 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 1999 Tipo de documento: Artigo