%0 Journal Article
%A Shimba, Akihiro
%A Cui, Guangwei
%A Abe, Shinya
%A Hirota, Keiji
%A Miyauchi, Eiji
%A Takami, Daichi
%A Tani-Ichi, Shizue
%A Kato, Ryoma
%A Tajima, Masaki
%A Kanahashi, Toru
%A Miyazaki, Masaki
%A Rodewald, Hans-Reimer
%A Yoshitomi, Hiroyuki
%A Ueno, Hideki
%A Ohno, Hiroshi
%A Ikuta, Koichi
%T Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells.
%J Cell reports
%V 44
%N 8
%@ 2211-1247
%C Maryland Heights, MO
%I Cell Press
%M DKFZ-2025-01616
%P 116093
%D 2025
%X Stress can trigger acute inflammation by increasing the pro-inflammatory cytokine interleukin (IL)-17 for injury and infection, while inducing the production of the immunosuppressive hormone glucocorticoids (GCs). However, the mechanism through which stress-induced GCs enhance acute inflammation by directly regulating the development of IL-17-producing helper T (Th17) cells remains unclear. Here, we demonstrate that GCs promote Th17 cell differentiation and survival in both mice and humans. Stress-induced GCs augment the expansion of Th17 cells expressing low levels of TCF1, a negative regulator of IL-17 expression. In addition, GCs promote Th17 cell differentiation by enhancing glycolysis. Stress-induced GCs also increase IL-17 production and neutrophil recruitment in the intestine upon bacterial antigen stimulation. Moreover, the expansion of Th17 cells mediated by stress-induced GCs exacerbates acute colitis by promoting IL-17 production and neutrophil recruitment. Thus, stress promotes acute inflammation by enhancing the differentiation of Th17 cells through GCs, which may contribute to self-defense against infections.
%K CP: Immunology (Other)
%K IL-17 (Other)
%K Th17 (Other)
%K colitis (Other)
%K glucocorticoid (Other)
%K neutrophil (Other)
%K stress (Other)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:40753571
%R 10.1016/j.celrep.2025.116093
%U https://inrepo02.dkfz.de/record/303366