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Peer-reviewedCC BYInternational journal of molecular sciences

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

  • Masaki Tajima1,2,3
  • Ivan J Fuss1
  • Naoko Ikuta3
  • Liming Mao1
  • Timothy G Myers4
  • Paul J Gardina4
  • Atsushi Kitani1
  • Warren Strober1
4 affiliations
  1. 1Mucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
  2. 2Division of Integrated High-Order Regulatory Systems, Center for Cancer Immunotherapy and Immunobiology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
  3. 3Department of Immunology, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe 650-0047, Japan.
  4. 4Genomic Technologies Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
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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 C. albicans renal infection. In addition, Dect-10 T cells, in accord with their IL-4-dependent genesis, suppress dust mite-induced experimental asthma.

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Cite

BibTeXRIS
BibTeX
@article{tajima2026glutaminolysis,
  title = {{Glutaminolysis and mTOR-C/EBPβ Signaling Drives the Differentiation of Novel IL-10-Producing Regulatory T Cells.}},
  author = {Masaki Tajima and Ivan J Fuss and Naoko Ikuta and Liming Mao and Timothy G Myers and Paul J Gardina and Atsushi Kitani and Warren Strober},
  journal = {International journal of molecular sciences},
  year = {2026},
  month = sep,
  doi = {10.3390/ijms27198447},
  url = {https://europepmc.org/article/MED/42883696},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Glutaminolysis and mTOR-C/EBPβ Signaling Drives the Differentiation of Novel IL-10-Producing Regulatory T Cells.
AU  - Masaki Tajima
AU  - Ivan J Fuss
AU  - Naoko Ikuta
AU  - Liming Mao
AU  - Timothy G Myers
AU  - Paul J Gardina
AU  - Atsushi Kitani
AU  - Warren Strober
PY  - 2026
DA  - 2026/09/22
JO  - International journal of molecular sciences
DO  - 10.3390/ijms27198447
UR  - https://europepmc.org/article/MED/42883696
AB  - 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 C. albicans renal infection. In addition, Dect-10 T cells, in accord with their IL-4-dependent genesis, suppress dust mite-induced experimental asthma.
SN  - 1422-0067
ER  -