Literature DB >> 28416440

Inhibition of the PI3K-Akt-mTOR signaling pathway in T lymphocytes in patients with active tuberculosis.

XueXuan Zhang1, TengYi Huang1, Ying Wu1, WenGuang Peng2, HanBin Xie2, MeiChen Pan1, HuanBin Zhou1, BoZhi Cai3, YingE Wu4.   

Abstract

OBJECTIVES: To investigate PI3K-Akt-mTOR signaling pathway changes and the proliferation of FoxP3+Treg cells in patients with active tuberculosis.
METHODS: We isolated PBMCs and CD4+CD25+FoxP3+Treg cells from peripheral blood collected from patients with active tuberculosis and healthy controls. We compared the proportion and MFI of PI3K-Akt-mTOR pathway components and PTEN by flow cytometry using specific cell-surface and intracellular markers. Moreover, we detected the specific secretory proteins ESAT-6 and Ag85B, cytokines IL-10, TGF-β1 and IL-35 in serum by ELISA.
RESULTS: Compared with healthy controls, the proportions of CD3+Akt+, CD3+p-Akt+, CD3+mTOR+, CD3+p-mTOR+ and CD3+PTEN+ cells, in the T lymphocyte population of patients with active tuberculosis, were decreased (p<0.05), while CD3+FoxP3+ cells were increased (p=0.013). Similarly, for CD4+CD25+FoxP3+Treg cells, the proportions of Akt+ cells, p-Akt+ cells, mTOR+ cells, p-mTOR+ cells and PTEN+ cells were decreased (p<0.05) in patients with active tuberculosis. Compared with healthy controls, the levels of ESAT-6 and Ag85B were higher in patients with active tuberculosis (p<0.001). Levels of IL-10 and TGF-β1 were higher (p<0.001), whereas the level of IL-35 was lower (p<0.001).
CONCLUSION: The PI3K-Akt-mTOR signaling pathway in T lymphocytes and CD4+CD25+FoxP3+Treg cells was inhibited, which could explain why M.tuberculosis can induce FoxP3+Treg cell to expand.
Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Entities:  

Keywords:  FoxP3(+)T(reg) cells; Mycobacterium tuberculosis; PI3K-Akt-mTOR pathway; T lymphocytes

Mesh:

Substances:

Year:  2017        PMID: 28416440     DOI: 10.1016/j.ijid.2017.04.004

Source DB:  PubMed          Journal:  Int J Infect Dis        ISSN: 1201-9712            Impact factor:   3.623


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