Evidence map›Paper›PMID 42875971›Full record

ArticleEuropean journal of immunology2026

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

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 and 3 more

Abstract read
In one paragraph

Article in European journal of immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Aleksandra Lopez KrolInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Luana SilvaInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Daniele C NascimentoInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Sophie M OberwalderInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Hitikk ChawlaInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Gabriel Alberto Barbosa de CarvalhoCenter for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Fatima BoukhalloukInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Monica RomeroInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Anne HausenInstitute of Pathology, University Medical Center Mainz, Mainz, Germany.
Matthias M GaidaInstitute of Pathology, University Medical Center Mainz, Mainz, Germany.
Luciana BerodResearch Center for Immunotherapy (FZI), University Medical Center, Johannes Gutenberg-University Mainz, Mainz, Germany.
José Carlos Alves-FilhoInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Tim SparwasserInstitute of Medical Microbiology and Hygiene, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.

Funding

German Research Foundation 318346496 CRC 1292 TP18German Research Foundation 490846870 CRC/TRR 355/1 A04German Research Foundation 490846870 CRC/TRR 355/1 B08German Research Foundation CRC 1292 TP22German Research Foundation TPQ1Gutenberg Research College Fellowship of the Johannes Gutenberg University MainzWilhelm-Sander Foundation r 2023.041.1
6 · The paper itself

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.

Indexed as

ColitisCyclic AMP Response Element ModulatorGlycolysisT-Lymphocytes, RegulatoryAnimalsCyclic AMPDextran SulfateForkhead Transcription FactorsInflammationInterferon-gammaLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutCyclic AMPCyclic AMP Response Element ModulatorDextran SulfateForkhead Transcription FactorsFoxp3 protein, mouseInterferon-gammacAMP metabolismDSS colitisglycolysisICER/CREMregulatory T cells

Identifiers

PMID42875971
PMCPMC13669413

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.