CD4+CD25+FoxP3+ regulatory T cells suppress Mycobacterium tuberculosis immunity in patients with active disease

被引:213
作者
Chen, Xinchun
Zhou, Boping
Li, Meizhong
Deng, Qunyi
Wu, Xueqiong
Le, Xiaohua
Wu, Chi
Larmonier, Nicolas
Zhang, Wei
Zhang, Hongmei
Wang, Huosheng
Katsanis, Emmanuel
机构
[1] Shenzhen Donghu Hosp, Shenzhen 518020, Peoples R China
[2] Univ Arizona, Steele Childrens Res Ctr, Dept Pediat, Tucson, AZ 85724 USA
[3] Guangdong Med Coll, Affiliated Shenzhen Hosp 3rd, Inst Hepatol, Shenzhen 518020, Peoples R China
[4] TB Ctr, Hosp PLA 309th, Beijing 100091, Peoples R China
基金
中国国家自然科学基金;
关键词
Mycobacterium tuberculosis; CD4(+)CD25(+)FoxP3(+) regulatory T cells; pulmonary tuberculosis;
D O I
10.1016/j.clim.2006.11.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CD4(+)CD25(+) regulatory T cells (Treg) play a central role in the prevention of autoimmunity and in the control of immune responses by down-regulating the function of effector CD4(+) or CD8(+) T cells. The role of Treg in Mycobacterium tuberculosis infection and persistence is inadequately documented. Therefore, the current study was designed to determine whether CD4(+)CD25(+)FoxP3(+) regulatory T cells may modulate immunity against human tuberculosis (TB). Our results indicate that the number of CD4(+)CD25(+)FoxP3(+) Treg increases in the blood or at the site of infection in active TB patients. The frequency of CD4(+)CD25(+)FoxP3(+) Treg in pleural. fluid inversely correlates with local MTB-specific immunity (p < 0.002). These CD4(+)CD25(+)FoxP3(+) T lymphocytes isolated from the blood and pleural fluid are capable of suppressing MTB-specific IFN-gamma and IL-10 production in TB patients. Therefore, CD4(+)CD25(+)FoxP3(+) Treg expanded in TB patients suppress M. tuberculosis immunity and may therefore contribute to the pathogenesis of human TB. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:50 / 59
页数:10
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