Stress-induced glucocorticoids enhance acute inflammation by promoting the differentiation of Th17 cells
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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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Altered glucocorticoid signaling can skew T-cell differentiation toward Th17 phenotypes, promoting their expansion and reinforcing downstream inflammatory cascades.
“Altered glucocorticoid signaling can skew T-cell differentiation toward Th17 phenotypes, promoting their expansion and reinforcing downstream inflammatory cascades [79]”
From Interorgan Communications in Skeletal Pathophysiology: From Molecular Pathways to Multidisciplinary Therapies (2026) · cites this paper as [79]
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Li, Y., Tan, Z., & Duan, J. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106668 · Cited by 3 · see citing works
Chen, J.-L., Liu, X., Zhao, H.-Y., Zhao, G.-H., & Gao, M.-D. (2025) · Scientific Reports · doi:10.1038/s41598-025-31533-w · Cited by 2 · see citing works
Feng, R., Huang, H., Ma, Q., Gao, W., Chen, X., Yan, X., Wang, F., Zhang, Q., Cao, Y., Zhang, H., et al. (2026) · Journal of Animal Science and Biotechnology/Journal of animal science and biotechnology · doi:10.1186/s40104-026-01401-2 · Cited by 2 · see citing works
Lv, Y., Lin, Y., Zheng, L., He, S., Huang, P., Wang, D., Zheng, X., & Fang, X. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.07.027 · Cited by 2 · see citing works
Gan, D., Qin, L., & Xiao, G. (2026) · Research · doi:10.34133/research.1319 · Cited by 1 · see citing works
“Altered glucocorticoid signaling can skew T-cell differentiation toward Th17 phenotypes, promoting their expansion and reinforcing downstream inflammatory cascades [ 79 ].”
Wang, J., Zhou, T.-S., Wu, H., & Liu, Y.-R. (2026) · Journal of Pharmacy and Pharmacology · doi:10.1093/jpp/rgag088 · Cited by 1 · see citing works
Piechowiak, P., & Lisowska, K. A. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262412041 · Cited by 1 · see citing works
Ren, S., Li, H., Dong, Z., & Fang, M. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1901065 · Cited by 1 · see citing works
Kyun, S., Kwon, G., Hwang, D., Jang, I., Kim, T., Park, H., Kim, S.-W., Lim, K., & Kim, J. (2025) · Physical Activity and Nutrition · doi:10.20463/pan.2025.0036
Ye, B., Yao, J., Wang, Y., Liao, X., Wu, D., Wang, M. X., Fang, X., Gao, J., Li, Q., & Gao, W. (2026) · Journal of Translational Medicine · doi:10.1186/s12967-026-08415-4
He, Y., Zhou, Z., Wei, X., Su, N., Yang, T., Wang, K., Yushan, L., Li, X., Hu, X., & Fu, Y. (2026) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2026.07.013
Sun, B., Han, F., Zhu, C., Yang, Z., Wang, H., 梅锦培, Chen, J., Zhu, J., Bo, Z., Wu, T., et al. (2026) · Advanced Science · doi:10.1002/advs.76681
Procházková, P., Knotková, H., Luthar, J., Roubalová, R., Kraus, M., Naghiyev, T., Patrono, E., Tlaskalová‐Hogenová, H., & Papežová, H. (2026) · Research Square · doi:10.21203/rs.3.rs-10776674/v1
Network Biology: Current Status, Applications, Challenges, and Future Prospects
Li, X., Zhang, L., Ding, Y., Li, K., Chang, S., Pei, L., Li, Z., & Chen, Z. (2026) · MedComm · doi:10.1002/mco2.71065
Intestinal toxicity and dysbiosis of microbiota in zebrafish (Danio rerio) exposed to prednisone
Cai, Q., Hu, X., Wu, J., Ye, M., Yang, J., Zeng, Y., Zheng, X., Chen, Y., Hou, L., Liu, R., et al. (2026) · Aquatic Toxicology · doi:10.1016/j.aquatox.2026.108051
- Authors
- Shimba, A., Cui, G., Abe, S., Hirota, K., Miyauchi, E., Takami, D., Tani-ichi, S., Kato, R., Tajima, M., Kanahashi, T., Miyazaki, M., Rodewald, H.-R., Yoshitomi, H., Ueno, H., Ohno, H., & Ikuta, K.
- Affiliations
- Kyoto University (JP)
- Gunma University (JP)
- German Cancer Research Center (DE)
- RIKEN (JP)
- Corresponding author
- Shimba, Akihiro
- Ikuta, Koichi
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2025-08
- Volume
- 44
- Issue
- 8
- Pages
- 116093
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W4412862202
- Cited by
- 15
- References
- 89
- Citations by year
- 2026: 12 · 2025: 3
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by)
- Kyoto University Research Information Repository (Kyoto University) (submittedVersion, cc-by)
- Funders
- Japan Agency for Medical Research and Development (JP22ama121034)
- Shimizu Foundation for Immunology and Neuroscience
- Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care
- Japan Society for the Promotion of Science (23H02735, 20K16284, 20K21525, 18K15184)
- Takeda Science Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- glucocorticoids, psychological stress, Th17 cells, IL-17, acute inflammation, TCF1, glycolysis, neutrophil recruitment, intestinal inflammation, colitis, bacterial infection, T helper cell differentiation
- MeSH terms
- Animals, Cell Differentiation, Colitis, Glucocorticoids, Humans, Inflammation, Male, Mice, Inbred C57BL, Stress, Physiological, Interleukin-17, Mice, Hepatocyte Nuclear Factor 1-alpha, Th17 Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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