The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Store-Operated Ca2+ Entry Controls Clonal Expansion of T Cells through Metabolic Reprogramming
Open accessAbstract
&NA; Store‐operated Ca2+ entry (SOCE) is the main Ca2+ influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca2+ release‐activated Ca2+ (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca2+‐dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impairs antigen‐dependent T cell proliferation. We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling glycolysis and oxidative phosphorylation. SOCE directs the metabolic reprogramming of naive T cells by regulating the expression of glucose transporters, glycolytic enzymes, and metabolic regulators through the activation of nuclear factor of activated T cells (NFAT) and the PI3K‐AKT kinase‐mTOR nutrient‐sensing pathway. We propose that SOCE controls a critical “metabolic checkpoint” at which T cells assess adequate nutrient supply to support clonal expansion and adaptive immune responses. Graphical Abstract Figure. No caption available. HighlightsSOCE regulates the clonal expansion of T cells and antiviral immunitySOCE and calcineurin induce glycolysis and oxidative phosphorylation in T cellsNFAT controls expression of glucose transporters, glycolytic enzymes, and regulatorsSOCE, calcineurin, and NFAT control a metabolic cell‐cycle checkpoint in T cells &NA; Clonal expansion of T cells is critical for protective immunity. Vaeth et al. (2017) demonstrate that store‐operated calcium entry (SOCE), calcineurin, and NFAT control cell‐cycle entry and proliferation of activated T cells through upregulation of glycolysis and oxidative phosphorylation.
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Cites
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
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Fueling Immunity: Insights into Metabolism and Lymphocyte Function
Pearce, E. L., Poffenberger, M. C., Chang, C.-H., & Jones, R. G. (2013) · Science · doi:10.1126/science.1242454 · Cited by 1,363
Calcium signalling in lymphocyte activation and disease
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Self-citationThe Transcription Factor NFAT Promotes Exhaustion of Activated CD8 + T Cells
Martinez, G. J., Pereira, R. M., Äijö, T., Kim, E. Y., Marangoni, F., Pipkin, M. E., Togher, S., Heissmeyer, V., Zhang, Y. C., Crotty, S., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.01.006 · Cited by 857 · cited 15×
“Deletion of NFATc1 and NFATc2 in T cells strongly impaired glycolytic gene expression, whereas expression of constitutively active NFATc1 in SOCE-deficient T cells restored glycolysis and T cell proliferation in vivo.”
InfluentialIon channels and transporters in lymphocyte function and immunity
Feske, S., Skolnik, E. Y., & Prakriya, M. (2012) · Nature Reviews Immunology · doi:10.1038/nri3233 · Cited by 441
Self-citationCalcineurin inhibitors: 40 years later, can’t live without
Azzi, J. R., Sayegh, M. H., & Mallat, S. G. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1390055 · Cited by 337
Inducible chromatin priming is associated with the establishment of immunological memory in T cells
Bevington, S. L., Cauchy, P., Piper, J., Bertrand, E., Lalli, N., Jarvis, R. C., Gilding, L. N., Ott, S., Bonifer, C., & Cockerill, P. N. (2016) · The EMBO Journal · doi:10.15252/embj.201592534 · Cited by 110
Cited by
Sun, L., Su, Y., Jiao, A., Wang, X., & Zhang, B. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01471-y · Cited by 1,014
Trebak, M., & Kinet, J.-P. (2019) · Nature Reviews Immunology · doi:10.1038/s41577-018-0110-7 · Cited by 508
Saravia, J., Chapman, N. M., & Chi, H. (2019) · Cellular & Molecular Immunology · doi:10.1038/s41423-019-0220-6 · Cited by 489
Reactive Oxygen Species: Involvement in T Cell Signaling and Metabolism
Franchina, D. G., Dostert, C., & Brenner, D. (2018) · Trends in Immunology · doi:10.1016/j.it.2018.01.005 · Cited by 322
Wu, H., Zhao, X., Hochrein, S. M., Eckstein, M., Gubert, G. F., Knöpper, K., Mansilla, A. M., Öner, A., Doucet-Ladevèze, R., Schmitz, W., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-42634-3 · Cited by 322
Self-citation
Metadata
- Authors
- Vaeth, M., Maus, M., Klein-Hessling, S., Freinkman, E., Yang, J., Eckstein, M., Cameron, S., Turvey, S. E., Serfling, E., Berberich-Siebelt, F., Possemato, R., & Feske, S.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 47
- Issue
- 4
- Pages
- 664-679.e6
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2763526200
- Cited by
- 276
- References
- 8
- FWCI
- 13.36
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Vaeth, M., Maus, M., Klein-Hessling, S., Freinkman, E., Yang, J., Eckstein, M., Cameron, S., Turvey, S. E., Serfling, E., Berberich-Siebelt, F., Possemato, R., & Feske, S. (2017). Store-Operated Ca2+ Entry Controls Clonal Expansion of T Cells through Metabolic Reprogramming. Immunity. https://doi.org/10.1016/j.immuni.2017.09.003
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