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Decrease in CD4+ CD25+ FoxP3+ Treg cells after pulmonary resection in the treatment of cavity multidrug-resistant tuberculosis

Summary Objectives Immune regulatory mechanisms may limit the immunopathologic condition of infection with Mycobacterium tuberculosis and suppress cellular immune responses in the host. We investigated the CD4+ CD25+ FoxP3+ circulating regulatory T cells (Treg ) in patients with cavity multidrug-res...

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Published in:International journal of infectious diseases 2010-09, Vol.14 (9), p.e815-e822
Main Authors: Wu, Ying E, Peng, Wen Guang, Cai, Ying Mu, Zheng, Gao Zhe, Zheng, Geng Long, Lin, Jing Hua, Zhang, Su Wei, Li, Ke
Format: Article
Language:English
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Summary:Summary Objectives Immune regulatory mechanisms may limit the immunopathologic condition of infection with Mycobacterium tuberculosis and suppress cellular immune responses in the host. We investigated the CD4+ CD25+ FoxP3+ circulating regulatory T cells (Treg ) in patients with cavity multidrug-resistant tuberculosis (MDR-TB) before and after surgery. Methods We compared the proportion of Treg cells in 13 patients with cavity MDR-TB pre- and postoperatively and in 10 healthy control subjects by flow cytometry using three specific markers in peripheral blood lymphocytes: cell-surface CD4 and CD25 expression and intracellular FoxP3 expression. Results The proportion of CD4+ CD25high and CD4+ CD25+ FoxP3+ Treg was significantly higher in patients with cavity MDR-TB and at 1-month postoperatively than in healthy controls ( p < 0.001). The proportion of CD4+ and CD4+ CD25− cells was significantly lower in patients with cavity MDR-TB than in controls ( p < 0.001). Pre- and postoperative proportions of CD4+ CD25high and CD4+ CD25+ FoxP3+ Treg cells showed a positive correlation ( r = 0.878, p < 0.001). Conclusion Circulating Treg cells are increased in proportion in patients with cavity MDR-TB and decreased after surgery. Infection with M. tuberculosis may induce Treg cell-surface molecular changes with increased numbers of cells.
ISSN:1201-9712
1878-3511
DOI:10.1016/j.ijid.2010.04.005