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

Haiju Zhang1, Yi Caudle2, Clay Wheeler2

  • 1Department of Pediatrics, Renmin Hospital of Wuhan University, Wuhan 430063, China; Department of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, TN 37614, United States.

Journal of Neuroimmunology
|November 25, 2017
PubMed

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.

Keywords:
Chronic stressFoxp3Immune suppressionSmad2/3TGF-β1TLR9

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