The Interleukin-2-mTORc1 Kinase Axis Defines the Signaling, Differentiation, and Metabolism of T Helper 1 and Follicular B Helper T Cells
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The differentiation of CD4(+) helper T cell subsets with diverse effector functions is accompanied by changes in metabolism required to meet their bioenergetic demands. We find that follicular B helper T (Tfh) cells exhibited less proliferation, glycolysis, and mitochondrial respiration, accompanied by reduced mTOR kinase activity compared to T helper 1 (Th1) cells in response to acute viral infection. IL-2-mediated activation of the Akt kinase and mTORc1 signaling was both necessary and sufficient to shift differentiation away from Tfh cells, instead promoting that of Th1 cells. These findings were not the result of generalized signaling attenuation in Tfh cells, because they retained the ability to flux calcium and activate NFAT-transcription-factor-dependent cytokine production. These data identify the interleukin-2 (IL-2)-mTORc1 axis as a critical orchestrator of the reciprocal balance between Tfh and Th1 cell fates and their respective metabolic activities after acute viral infection.
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CD25 is the upstream molecule inducing mTOR signaling in T cells.
“Recently, CD25 was shown to be the upstream molecule inducing mTOR signaling in T cells42”
From Microbial short-chain fatty acids modulate CD8+ T cell responses and improve adoptive immunotherapy for cancer (2021) · cites this paper as [42]
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Follicular Helper CD4 T Cells (T <sub>FH</sub> )
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- Authors
- Ray, J. P., Staron, M. M., Shyer, J. A., Ho, P.-C., Marshall, H. D., Gray, S. M., Laidlaw, B. J., Araki, K., Ahmed, R., Kaech, S. M., & Craft, J.
- Affiliations
- Yale University (US)
- Emory University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Kaech, Susan M.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 43
- Issue
- 4
- Pages
- 690-702
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC4618086
- OpenAlex
- W1963232095
- Cited by
- 315
- References
- 59
- Citations by year
- 2026: 14 · 2025: 29 · 2024: 28 · 2023: 28 · 2022: 25 · 2021: 33 · 2020: 28 · 2019: 28 · 2018: 33 · 2017: 34 · 2016: 34 · 2015: 1
- FWCI
- 16.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM007205)
- National Institute of Allergy and Infectious Diseases (R01AI139675, AI075157, R01AI075157, F32AI094791, R01AI066232)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR063942, AR063942, R21AR062842, P30AR053495, AR 40072, R01AR040072, AR062842, R21AR068662, AR053495, R37AR040072)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- interleukin-2, mTORC1, Th1 cells, T cell differentiation, T cell metabolism, glycolysis, mitochondrial respiration, Akt signaling, acute viral infection, NFAT, calcium signaling, cytokine production
- MeSH terms
- Positive Regulatory Domain I-Binding Factor 1, Mechanistic Target of Rapamycin Complex 1, Animals, Cell Cycle, Cell Division, Enzyme Activation, Glucose, Glycolysis, T-Lymphocytes, Helper-Inducer, Interleukin-2, Lymphocytic choriomeningitis virus, Mice, Inbred C57BL, Oxygen Consumption, Specific Pathogen-Free Organisms, Transcription Factors, Signal Transduction, T-Lymphocyte Subsets, Apoptosis, Th1 Cells, Calcium Signaling, Multiprotein Complexes, NFATC Transcription Factors, Proto-Oncogene Proteins c-akt, Interleukin-2 Receptor alpha Subunit, TOR Serine-Threonine Kinases
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