The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
The Transcription Factor FoxO1 Sustains Expression of the Inhibitory Receptor PD-1 and Survival of Antiviral CD8+ T Cells during Chronic Infection
Open accessAbstract
Summary Protein kinase B (a.k.a. AKT) and the mechanistic target of rapamycin (mTOR) are central regulators of T cell differentiation, proliferation, metabolism and survival. Here, we show that during chronic murine lymphocytic choriomeningitis virus (LCMV) infection, activation of AKT and mTOR are impaired in antiviral cytotoxic T lymphocytes (CTLs), resulting in enhanced activity of the transcription factor FoxO1. Blockade of inhibitory receptor programmed cell death protein 1 (PD-1) in vivo increased mTOR activity in virus-specific CTLs, and its therapeutic effects were abrogated by the mTOR inhibitor rapamycin. FoxO1 functioned as a transcriptional activator of PD-1 that promoted the differentiation of terminally exhausted CTLs. Importantly, FoxO1 null CTLs failed to persist and control chronic viral infection. Collectively, this study identifies that CTLs adapt to persistent infection through a positive feedback pathway (PD-1→FoxO1→PD-1) that functions to both desensitize virus-specific CTLs to antigen and to support their survival during chronic viral infection.
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Citations
Cites
PD-1 and Its Ligands in Tolerance and Immunity
Keir, M. E., Butte, M. J., Freeman, G. J., & Sharpe, A. H. (2008) · Annual Review of Immunology · doi:10.1146/annurev.immunol.26.021607.090331 · Cited by 5,378
Wherry, E. J. (2011) · Nature Immunology · doi:10.1038/ni.2035 · Cited by 4,062 · cited 5×
“The persistence of antigen can lead to alterations in cytotoxic T lymphocyte (CTL) proliferation, survival, effector functions, and gene expression that lead to the differentiation of dysfunctional or ‘‘exhausted’’ CTLs (Wherry, 2011).”
BackgroundInfluentialThe transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
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“Additionally, activation of PI3K, AKT, and mTOR signaling can induce a metabolic switch towards anabolic metabolism and aerobic glycolysis in activated CD8+ T cells that is transcriptionally coordinated in part by c-myc and hypoxia inducible factor-1 (HIF-1) (Doedens et al., 2013; Finlay et al., 2012; Frauwirth et al.…”
BackgroundInfluentialMetabolic Pathways in Immune Cell Activation and Quiescence
Pearce, E. L., & Pearce, E. J. (2013) · Immunity · doi:10.1016/j.immuni.2013.04.005 · Cited by 1,692
mTOR regulates memory CD8 T-cell differentiation
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Enhancing CD8 T-cell memory by modulating fatty acid metabolism
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The CD28 Signaling Pathway Regulates Glucose Metabolism
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“Additionally, activation of PI3K, AKT, and mTOR signaling can induce a metabolic switch towards anabolic metabolism and aerobic glycolysis in activated CD8+ T cells that is transcriptionally coordinated in part by c-myc and hypoxia inducible factor-1 (HIF-1) (Doedens et al., 2013; Finlay et al., 2012; Frauwirth et al.…”
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Exhaustion of tumor-specific CD8+ T cells in metastases from melanoma patients
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Cited by
Molecular and cellular insights into T cell exhaustion
Wherry, E. J., & Kurachi, M. (2015) · Nature Reviews Immunology · doi:10.1038/nri3862 · Cited by 4,652
Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression
Chang, C.-H., Qiu, J., O’Sullivan, D., Buck, M. D., Noguchi, T., Curtis, J. D., Chen, Q., Gindin, M., Gubin, M. M., van der Windt, G. J. W., et al. (2015) · Cell · doi:10.1016/j.cell.2015.08.016 · Cited by 3,331
Phosphoenolpyruvate Is a Metabolic Checkpoint of Anti-tumor T Cell Responses
Ho, P.-C., Bihuniak, J. D., Macintyre, A. N., Staron, M., Liu, X., Amezquita, R., Tsui, Y.-C., Cui, G., Micevic, G., Perales, J. C., et al. (2015) · Cell · doi:10.1016/j.cell.2015.08.012 · Cited by 1,462
Self-citationEpigenetic stability of exhausted T cells limits durability of reinvigoration by PD-1 blockade
Pauken, K. E., Sammons, M. A., Odorizzi, P. M., Manne, S., Godec, J., Khan, O., Drake, A. M., Chen, Z., Sen, D. R., Kurachi, M., et al. (2016) · Science · doi:10.1126/science.aaf2807 · Cited by 1,348
Thommen, D. S., & Schumacher, T. N. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.012 · Cited by 1,299
Metadata
- Authors
- Staron, M. M., Gray, S. M., Marshall, H. D., Parish, I. A., Chen, J. H., Perry, C. J., Cui, G., Li, M. O., & Kaech, S. M.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 41
- Issue
- 5
- Pages
- 802-814
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1992581811
- Cited by
- 385
- References
- 19
- FWCI
- 11.80
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Staron, M. M., Gray, S. M., Marshall, H. D., Parish, I. A., Chen, J. H., Perry, C. J., Cui, G., Li, M. O., & Kaech, S. M. (2014). The Transcription Factor FoxO1 Sustains Expression of the Inhibitory Receptor PD-1 and Survival of Antiviral CD8+ T Cells during Chronic Infection. Immunity. https://doi.org/10.1016/j.immuni.2014.10.013
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