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

Authors

Aleksandra Lopez Krol, Luana Silva, Daniele C Nascimento, Sophie M Oberwalder, Hitikk Chawla, Gabriel Alberto Barbosa de Carvalho, Fatima Boukhallouk, Monica Romero, Anne Hausen, Matthias M Gaida, Luciana Berod, José Carlos Alves-Filho, Tim Sparwasser

Published in

European journal of immunology. Volume 56. Issue 10. Pages e70297.

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.

PMID:
42875971
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.

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