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Multidrug-resistant Mycobacteriu m tuberculosis (MDR-TB) patients often causes persistent infection and chemotherapy failure, which brings heavy burden to society and family.Many immune cell subsets and regulatory mechanisms may operate throughout the various stages of infection.The presence of regulatory T (Treg) cells is thought to be an important mechanism by which TB successfully evades the immune system.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 NK cells.The role of Tregs in MDR-TB infection and persistence is inadequately documented yet.Therefore, the current study was designed to determine whether CD4+CD25+CD127low regulatory T cells may modulate innate immunity (such as NK cells) against human tuberculosis (TB).Our results indicated that the number of CD4+CD25+CD127low Treg cells increased in multidrug-resistant TB patients blood.The cytokine production of TGF-betal and IFN-γ was increased in MDR-patients with culture and sputum smear-positive pulmonary TB (PTB+) compared with healthy subjects, along with the lowest activity and CD69 of NK cells in patients and controls.Down-regulation of Treg cells increased CD69 expression and NK cells activity.These results suggested that immunity to MDR-patients induced circulating CD4+CD25+CD127low cell expansion, which may be related to the progression of M.tuberculosis infection, and that the balance between effectors immune responses and suppression immune responses.