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TGF-β1/Smad2/3/Foxp3 signaling is required for chronic stress-induced immune suppression.

Abstract：

:Depending on the duration and severity, psychological tension and physical stress can enhance or suppress the immune system in both humans and animals. Although it has been established that chronic stress exerts a significant suppressive effect on immune function, the mechanisms by which affects immune responses remain elusive. By employing an in vivo murine system, we revealed that TGF-β1/Smad2/3/Foxp3 axis was remarkably activated following chronic stress. Furthermore, TLR9 and p38 MAPK played a critical role in the activation of TGF-β1/Smad2/3/Foxp3 signaling cascade. Moreover, inhibition of TGF-β1/Smad2/3/Foxp3 or p38 significantly attenuated chronic stress-induced lymphocyte apoptosis and apoptosis-related proteins, as well as the differentiation of T regulatory cells in spleen. Interestingly, disequilibrium of pro-inflammatory and anti-inflammatory cytokines balance caused by chronic stress was also rescued by blocking TGF-β1/Smad2/3/Foxp3 axis. These findings yield insight into a novel mechanism by which chronic stress modulates immune functions and identifies new targets for the development of novel anti-immune suppressant medications.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Zhang H,Caudle Y,Wheeler C,Zhou Y,Stuart C,Yao B,Yin D

doi

10.1016/j.jneuroim.2017.11.005

subject

Has Abstract

pub_date

2018-01-15 00:00:00

pages

30-41

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(17)30465-4

journal_volume

314

pub_type

杂志文章

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