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| 001 | 303366 | ||
| 005 | 20250810021951.0 | ||
| 024 | 7 | _ | |a 10.1016/j.celrep.2025.116093 |2 doi |
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| 100 | 1 | _ | |a Shimba, Akihiro |b 0 |
| 245 | _ | _ | |a Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells. |
| 260 | _ | _ | |a Maryland Heights, MO |c 2025 |b Cell Press |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1754316176_1839 |2 PUB:(DE-HGF) |
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| 520 | _ | _ | |a 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. |
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| 650 | _ | 7 | |a CP: Immunology |2 Other |
| 650 | _ | 7 | |a IL-17 |2 Other |
| 650 | _ | 7 | |a Th17 |2 Other |
| 650 | _ | 7 | |a colitis |2 Other |
| 650 | _ | 7 | |a glucocorticoid |2 Other |
| 650 | _ | 7 | |a neutrophil |2 Other |
| 650 | _ | 7 | |a stress |2 Other |
| 700 | 1 | _ | |a Cui, Guangwei |b 1 |
| 700 | 1 | _ | |a Abe, Shinya |b 2 |
| 700 | 1 | _ | |a Hirota, Keiji |b 3 |
| 700 | 1 | _ | |a Miyauchi, Eiji |b 4 |
| 700 | 1 | _ | |a Takami, Daichi |b 5 |
| 700 | 1 | _ | |a Tani-Ichi, Shizue |b 6 |
| 700 | 1 | _ | |a Kato, Ryoma |b 7 |
| 700 | 1 | _ | |a Tajima, Masaki |b 8 |
| 700 | 1 | _ | |a Kanahashi, Toru |b 9 |
| 700 | 1 | _ | |a Miyazaki, Masaki |b 10 |
| 700 | 1 | _ | |a Rodewald, Hans-Reimer |0 P:(DE-He78)86fa3316b7be0d661065d02b3baec3d6 |b 11 |u dkfz |
| 700 | 1 | _ | |a Yoshitomi, Hiroyuki |b 12 |
| 700 | 1 | _ | |a Ueno, Hideki |b 13 |
| 700 | 1 | _ | |a Ohno, Hiroshi |b 14 |
| 700 | 1 | _ | |a Ikuta, Koichi |b 15 |
| 773 | _ | _ | |a 10.1016/j.celrep.2025.116093 |g Vol. 44, no. 8, p. 116093 - |0 PERI:(DE-600)2649101-1 |n 8 |p 116093 |t Cell reports |v 44 |y 2025 |x 2211-1247 |
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