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@ARTICLE{Shimba:303366,
      author       = {A. Shimba and G. Cui and S. Abe and K. Hirota and E.
                      Miyauchi and D. Takami and S. Tani-Ichi and R. Kato and M.
                      Tajima and T. Kanahashi and M. Miyazaki and H.-R.
                      Rodewald$^*$ and H. Yoshitomi and H. Ueno and H. Ohno and K.
                      Ikuta},
      title        = {{S}tress-induced glucocorticoids enhance acute inflammation
                      by promoting the differentiation of {T}h17 cells.},
      journal      = {Cell reports},
      volume       = {44},
      number       = {8},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-01616},
      pages        = {116093},
      year         = {2025},
      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.},
      keywords     = {CP: Immunology (Other) / IL-17 (Other) / Th17 (Other) /
                      colitis (Other) / glucocorticoid (Other) / neutrophil
                      (Other) / stress (Other)},
      cin          = {D110},
      ddc          = {610},
      cid          = {I:(DE-He78)D110-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40753571},
      doi          = {10.1016/j.celrep.2025.116093},
      url          = {https://inrepo02.dkfz.de/record/303366},
}