Autoantibodies against the second extracellular loop ofβ1-adrenoceptor from patients with DCM in-hibit the proliferation of CD4+T lymphocytes byβ1-adrenoceptor / 中华微生物学和免疫学杂志
Chinese Journal of Microbiology and Immunology
;
(12): 518-524, 2013.
Artigo
em Chinês
| WPRIM
| ID: wpr-438292
ABSTRACT
Objective To investigate the effects of autoantibodies (β1-AA) against second extra-cellular loop of the β1-adrenergic receptor (β1-AR-ECⅡ) in sera of patients with dilated cardiomyopathy (DCM) on proliferation of rat CD4+T lymphocytes.Methods β1-AA in the sera of patients with DCM was purified by affinity chromatography .CD4+T lymphocytes were isolated by immunomagnetic microbeads from peripheral blood mononuclear cells of rats and its positive rate was detected by flow cytometry .CCK-8 meth-od was used to detect the proliferation of CD 4+T lymphocytes and flow cytometry was performed to measure the ratio of CD4+/CD8+T lymphocyte .Results The purity of isolated rat CD 4+T lymphocytes by immu-nomagnetic microbeads reached 97.7%.The proliferation of CD4+T lymphocytes stimulated by CD3/CD28 was inhibited by β1-AA in a concentration-dependent manner .However , IgG antibodies extracted from sera of healthy controls did not suppress lymphocyte proliferation (P>0.05).The suppression effect of β1-AA was inhibited after binding to antigenic peptides corresponding to β1-AR-ECⅡ and was completely blocked by metoprolol, a specific antagonist of β1-adrenergic receptor (β1-AR).In addition,β1-AA had no effects on the ratio of CD4+/CD8+T lymphocyte .Conclusion β1-AA isolated from DCM patients suppresses the pro-liferation of CD4+T lymphocytes through β1-AR pathway , which indicates that β1-AA can directly reduce the number of T lymphocytes and impair the function of T lymphocytes , resulting in immune system disorders and the development of DCM .
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Microbiology and Immunology
Ano de publicação:
2013
Tipo de documento:
Artigo
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