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Peer-reviewedCC BYEuropean journal of immunology

Inducible cAMP Early Repressor Limits Glycolytic Programming in Regulatory T Cells and Supports Control of Inflammatory Colitis.

  • Aleksandra Lopez Krol1
  • Luana Silva1
  • Daniele C Nascimento1
  • Sophie M Oberwalder1
  • Hitikk Chawla1
  • Gabriel Alberto Barbosa de Carvalho2
  • Fatima Boukhallouk1
  • Monica Romero1
  • Anne Hausen3
  • Matthias M Gaida3,4,5
  • Luciana Berod5,6
  • José Carlos Alves-Filho1,2
1 more authors
  • Tim Sparwasser1,5
6 affiliations
  1. 1Institute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
  2. 2Center for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
  3. 3Institute of Pathology, University Medical Center Mainz, Mainz, Germany.
  4. 4Translational Oncology at the University Medical Center Mainz (TRON), Mainz, Germany.
  5. 5Research Center for Immunotherapy (FZI), University Medical Center, Johannes Gutenberg-University Mainz, Mainz, Germany.
  6. 6Institute of Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
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Abstract

Regulatory T cells (Tregs) are essential for immune tolerance, with cAMP metabolism central to their suppressive function. Inducible cAMP early repressor (ICER) is a negative regulator of cAMP signalling. However, its role in Treg biology is not fully understood. Here we generated Foxp3-specific ICER knockout mice to assess ICER's function in Tregs. We found that ICER deficiency does not impair Treg development or suppression of effector T cell proliferation under homeostatic conditions. However, ICER-deficient Tregs display enhanced Foxp3 stability, increased glycolysis and proliferation but exhibit impaired suppression of IFN-γ production by effector T cells. In a dextran sodium sulphate-induced colitis model, loss of ICER in Tregs led to aggravated intestinal inflammation and tissue damage, without, however, a marked effect on gross disease parameters. These results identify ICER as a context-dependent modulator of Treg metabolism and inflammatory cytokine control, highlighting its potential role in regulating immune responses during inflammation.

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Cite

BibTeXRIS
BibTeX
@article{krol2026inducible,
  title = {{Inducible cAMP Early Repressor Limits Glycolytic Programming in Regulatory T Cells and Supports Control of Inflammatory Colitis.}},
  author = {Aleksandra Lopez Krol and Luana Silva and Daniele C Nascimento and Sophie M Oberwalder and Hitikk Chawla and Gabriel Alberto Barbosa de Carvalho and Fatima Boukhallouk and Monica Romero and Anne Hausen and Matthias M Gaida and Luciana Berod and José Carlos Alves-Filho and Tim Sparwasser},
  journal = {European journal of immunology},
  year = {2026},
  month = oct,
  doi = {10.1002/eji.70297},
  url = {https://europepmc.org/article/MED/42875971},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Inducible cAMP Early Repressor Limits Glycolytic Programming in Regulatory T Cells and Supports Control of Inflammatory Colitis.
AU  - Aleksandra Lopez Krol
AU  - Luana Silva
AU  - Daniele C Nascimento
AU  - Sophie M Oberwalder
AU  - Hitikk Chawla
AU  - Gabriel Alberto Barbosa de Carvalho
AU  - Fatima Boukhallouk
AU  - Monica Romero
AU  - Anne Hausen
AU  - Matthias M Gaida
AU  - Luciana Berod
AU  - José Carlos Alves-Filho
AU  - Tim Sparwasser
PY  - 2026
DA  - 2026/10/01
JO  - European journal of immunology
DO  - 10.1002/eji.70297
UR  - https://europepmc.org/article/MED/42875971
AB  - Regulatory T cells (Tregs) are essential for immune tolerance, with cAMP metabolism central to their suppressive function. Inducible cAMP early repressor (ICER) is a negative regulator of cAMP signalling. However, its role in Treg biology is not fully understood. Here we generated Foxp3-specific ICER knockout mice to assess ICER's function in Tregs. We found that ICER deficiency does not impair Treg development or suppression of effector T cell proliferation under homeostatic conditions. However, ICER-deficient Tregs display enhanced Foxp3 stability, increased glycolysis and proliferation but exhibit impaired suppression of IFN-γ production by effector T cells. In a dextran sodium sulphate-induced colitis model, loss of ICER in Tregs led to aggravated intestinal inflammation and tissue damage, without, however, a marked effect on gross disease parameters. These results identify ICER as a context-dependent modulator of Treg metabolism and inflammatory cytokine control, highlighting its potential role in regulating immune responses during inflammation.
SN  - 0014-2980
SN  - 1521-4141
ER  -