Journal Article DKFZ-2025-01616

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Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells.

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2025
Cell Press Maryland Heights, MO

Cell reports 44(8), 116093 () [10.1016/j.celrep.2025.116093]
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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

Classification:

Contributing Institute(s):
  1. Zelluläre Immunologie (D110)
Research Program(s):
  1. 314 - Immunologie und Krebs (POF4-314) (POF4-314)

Appears in the scientific report 2025
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Medline ; DOAJ ; Article Processing Charges ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; DOAJ Seal ; Essential Science Indicators ; Fees ; IF >= 5 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection
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 Record created 2025-08-04, last modified 2025-08-10



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