Author/Authors :
Chen، نويسنده , , Xinchun and Zhou، نويسنده , , Boping and Li، نويسنده , , Meizhong and Deng، نويسنده , , Qunyi and Wu، نويسنده , , Xueqiong and Le، نويسنده , , Xiaohua and Wu، نويسنده , , Chi and Larmonier، نويسنده , , Nicolas and Zhang، نويسنده , , Wei and Zhang، نويسنده , , Hongmei and Wang، نويسنده , , Huosheng and Katsanis، نويسنده , , Emmanuel، نويسنده ,
Abstract :
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-γ 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.
