Literature DB >> 18060626

Changes of CD4+CD25+ regulatory T cells in patients with acute coronary syndrome and the effects of atorvastatin.

Zhenping Hu1, Dazhu Li, Yingfeng Hu, Keping Yang.   

Abstract

The function of CD4(+)CD25(+) regulatory T lymphocytes (Treg) in patients with acute coronary syndrome (ACS) and the effects of atorvastatin were investigated. Forty-eight patients with ACS were randomly divided into two groups: group C receiving conventional therapy (n=24), and group C+A receiving conventional therapy+atorvastatin (10 mg/day, n=24). T lymphocytes from ACS patients (before and 2 weeks after the treatment) or 18 healthy subjects were separated and the flow cytometry was used to measure the percentage of Treg. The inhibitory ability of Treg on effector T cells was determined by mixed lymphocyte reaction (MLR). ELISA was used to measure the serum levels of cytokines (IL-10, TGF-beta1 and IFN-gamma) before and after treatment. The results showed that as compared with normal control group, Treg percentage was decreased significantly (P<0.01), the inhibitory ability of Treg on the T lymphocytes proliferation was reduced (P<0.01), IFN-gamma levels were increased and IL-10 and TGF-beta1 levels were lowered in ACS patients. After treatment with atorvastatin, Treg percentage and the inhibitory ability of Treg on T lymphocytes proliferation were significantly increased in ACS patients. Serum IFN-gamma was decreased significantly, while IL-10 and TGF-beta1 were elevated significantly as compared with the non-atorvastatin group. The number of Treg was positively correlated with serum TGF-beta1, but negatively with serum IFN-gamma and CRP. It was concluded that ACS was associated with decreased number and defected function of Treg, which may play an important role in initiating immune-inflammatory response in ACS. The inhibitory effects of atorvastatin on inflammation in ACS may be due to its beneficial effects on Treg and restoration of immune homeostasis.

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Year:  2007        PMID: 18060626     DOI: 10.1007/s11596-007-0512-4

Source DB:  PubMed          Journal:  J Huazhong Univ Sci Technolog Med Sci        ISSN: 1672-0733


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