Glutaminolysis and mTOR-C/EBPβ Signaling Drives the Differentiation of Novel IL-10-Producing Regulatory T Cells.

Masaki Tajima, Ivan J Fuss, Naoko Ikuta, Liming Mao, Timothy G Myers, Paul J Gardina, Atsushi Kitani, Warren Strober

Abstract read

In one paragraph

Article in International journal of molecular sciences, 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

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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

8 authors.

Masaki TajimaMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-3407-0229

Ivan J FussMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Naoko IkutaDepartment of Immunology, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe 650-0047, Japan.

Liming MaoMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Timothy G MyersGenomic Technologies Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-7059-5906

Paul J GardinaGenomic Technologies Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Atsushi KitaniMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-7628-1716

Warren StroberMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Funding

Japan Society for the Promotion of Science 19K16881Japan Society for the Promotion of Science 24K10092NIH HHS

6 · The paper itself

Abstract

Here we report that Dectin-1-stimulated dendritic cells (DCs) induce unique IL-10-producing T cells with strong regulatory function during fungal infection or experimental asthma. These T cells, which we call Dect-10 T cells, are induced by DC-initiated signaling that sets in motion two complementary mechanisms of IL-10-producing T cell differentiation. The first involves induction of nascent Dect-10 T cell IL-4 synthesis and attendant GATA3 production, the latter being a factor that exerts canonical and epigenetic transcriptional function at separate IL-10 promoter sites. The second involves TGFβ superfamily signaling associated with induction of glutaminolysis and generation of alpha-ketoglutarate, a factor that induces rapamycin-sensitive TORC1 activation; in turn, such activation causes the translation of the LIP isoform of C/EBPβ and the formation of a CREB1-LIP complex that binds to adjacent sites on the IL-10 promoter to facilitate the transactivation of the IL10 gene. Dect-10 T cell regulatory function is manifested through its capacity to down-regulate normally protective immune responses to hyphal

Indexed as

CCAAT-Enhancer-Binding Protein-betaCell DifferentiationInterleukin-10Signal TransductionT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesAnimalsAsthmaCandida albicansCyclic AMP Response Element-Binding ProteinDendritic CellsInterleukin-4Lectins, C-TypeMicePromoter Regions, GeneticTransforming Growth Factor betaCCAAT-Enhancer-Binding Protein-betaCyclic AMP Response Element-Binding ProteinInterleukin-10Interleukin-4Lectins, C-TypeTOR Serine-Threonine KinasesTransforming Growth Factor betaActRIB (ALK4)asthmaC. albicans infectionC-type lectinsglutaminolysisIL-10mTOR

Identifiers

PMID42883696

DOI10.3390/ijms27198447

PMCPMC13664842

What OpenQuestion holds

Textmetadata

Read underepoch 390

Registered trials

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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.