Home > Publications database > Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells. |
Journal Article | DKFZ-2025-01616 |
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2025
Cell Press
Maryland Heights, MO
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Please use a persistent id in citations: doi:10.1016/j.celrep.2025.116093
Abstract: 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.
Keyword(s): CP: Immunology ; IL-17 ; Th17 ; colitis ; glucocorticoid ; neutrophil ; stress
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