TY - JOUR
AU - Shimba, Akihiro
AU - Cui, Guangwei
AU - Abe, Shinya
AU - Hirota, Keiji
AU - Miyauchi, Eiji
AU - Takami, Daichi
AU - Tani-Ichi, Shizue
AU - Kato, Ryoma
AU - Tajima, Masaki
AU - Kanahashi, Toru
AU - Miyazaki, Masaki
AU - Rodewald, Hans-Reimer
AU - Yoshitomi, Hiroyuki
AU - Ueno, Hideki
AU - Ohno, Hiroshi
AU - Ikuta, Koichi
TI - Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells.
JO - Cell reports
VL - 44
IS - 8
SN - 2211-1247
CY - Maryland Heights, MO
PB - Cell Press
M1 - DKFZ-2025-01616
SP - 116093
PY - 2025
AB - 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.
KW - CP: Immunology (Other)
KW - IL-17 (Other)
KW - Th17 (Other)
KW - colitis (Other)
KW - glucocorticoid (Other)
KW - neutrophil (Other)
KW - stress (Other)
LB - PUB:(DE-HGF)16
C6 - pmid:40753571
DO - DOI:10.1016/j.celrep.2025.116093
UR - https://inrepo02.dkfz.de/record/303366
ER -