Open AccessTLR2 Involved in Naive CD4+ T Cells Rescues Stress-Induced Immune Suppression by Regulating Th1/Th2 and Th17
Author(s) -
Jing Zhao,
Jing Liu,
James Denney,
Chen Li,
Fang Li,
Fen Chang,
Mingyou Chen,
Deling Yin
Publication year - 2015
Publication title -
neuroimmunomodulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.635
H-Index - 65
eISSN - 1423-0216
pISSN - 1021-7401
DOI - 10.1159/000371468
Subject(s) - immune system , tlr2 , immunology , tumor necrosis factor alpha , cytokine , biology , p38 mitogen activated protein kinases , mapk/erk pathway , interleukin 12 , microbiology and biotechnology , interleukin 21 , cytotoxic t cell , t cell , signal transduction , innate immune system , in vitro , biochemistry
Stress, either physical or psychological, can have a dramatic impact on our immune system. There has been little progress, however, in understanding chronic stress-induced immunosuppression. Naive CD4+ T cells could modulate immune responses via differentiation to T helper (Th) cells. In this study, we showed that stress promotes the release of the Th1 cytokines interferon (IFN)-γ and tumor necrosis factor (TNF)-α, the Th2 cytokines interleukin (IL)-4 and IL-10 and the Th17 cytokine IL-17 of splenic naive CD4+ T cells. This suggests that stress promotes the differentiation of naive CD4+ T cells to Th1, Th2 and Th17 cells. Knockout strategies verified that TLR2 might modulate the differentiation of Th1/Th2 cells by inhibiting p38 mitogen-activated protein kinase (MAPK). Taken together, our data suggest that chronic stress induces immune suppression by targeting TLR2 and p38 MAPK in naive CD4+ T cells.