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在慢性猴免疫缺陷病毒感染期间,调节性 T 细胞的抑制活性与高 CD4(+) T 细胞计数和低 T 细胞活化相关。

Suppressive activity of regulatory T cells correlates with high CD4(+) T-cell counts and low T-cell activation during chronic simian immunodeficiency virus infection.

机构信息

CEA, Division of Immuno-Virology, Institute of Emerging Diseases and Innovative Therapies, Fontenay-aux-Roses, France.

出版信息

AIDS. 2011 Mar 13;25(5):585-93. doi: 10.1097/QAD.0b013e3283437c7b.

Abstract

OBJECTIVE

HIV/simian immunodeficiency virus (SIV) infection is characterized by progressive CD4(+) T-cell depletion and immune exhaustion. CD25(+)FoxP3(+) regulatory T cells were evidenced in HIV/SIV infection and disease. They could be positive by suppressing immune activation during chronic infection and/or damper T-cell immunity. Here we evaluated the correlation between regulatory T-cell function and disease progression in pathogenic SIV infection.

DESIGN

We compared the in-vitro suppressive capacity of CD25(+) cells from peripheral blood and peripheral lymph nodes of 18 SIVmac251-infected cynomolgus macaques to look for correlates with biological markers of progression to disease.

METHODS

The in-vitro suppressive capacity of CD25(+) cells was evaluated in a proliferation assay. Ex-vivo T-cell activation was determined by phenotypic labeling followed by flow cytometry.

RESULTS

In chronic infection, CD25(+) regulatory T-cell activity correlated to preserved CD4 T-cell counts and lower T-cell activation.

CONCLUSION

This study suggests that regulatory T-cell function is lost during disease progression and may have a positive impact on HIV/SIV disease.

摘要

目的

人类免疫缺陷病毒/猴免疫缺陷病毒(SIV)感染的特征是 CD4(+)T 细胞进行性耗竭和免疫衰竭。在 HIV/SIV 感染和疾病中已经证实存在 CD25(+)FoxP3(+)调节性 T 细胞。它们可以通过在慢性感染期间抑制免疫激活和/或抑制 T 细胞免疫而呈阳性。在此,我们评估了调节性 T 细胞功能与致病性 SIV 感染疾病进展之间的相关性。

设计

我们比较了 18 只感染 SIVmac251 的食蟹猴外周血和外周淋巴结中 CD25(+)细胞的体外抑制能力,以寻找与疾病进展的生物学标志物相关的指标。

方法

通过增殖测定评估 CD25(+)细胞的体外抑制能力。通过表型标记后进行流式细胞术测定体外 T 细胞激活。

结果

在慢性感染中,CD25(+)调节性 T 细胞的活性与 CD4 T 细胞计数的保存和 T 细胞激活的降低相关。

结论

本研究表明,调节性 T 细胞功能在疾病进展过程中丧失,可能对 HIV/SIV 疾病产生积极影响。

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