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Intersection of mTOR and STAT signaling in immunity
Open accessAbstract
Optimal regulation of immune networks is essential for the generation of effective immune responses, and defects in such networks can lead to immunodeficiency while uncontrolled responses can result in autoimmune disorders. mTOR and STAT signaling cascades are key regulators of the differentiation and function of cells of the immune system. Both pathways act as sensors and transducers of environmental stimuli, and recent evidence has revealed points of crosstalk between these pathways, highlighting synergistic regulation of immune cell differentiation and function. We review here the current understanding of mTOR and STAT interactions in T cells and innate immune cells, and discuss potential mechanisms underlying these events. We further outline models for the intersection of these pathways in the regulation of immunity and highlight important areas for future research.
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“mTOR has also been shown to regulate STAT signaling175, and studies in older humans show that the elevation in baseline phosphorylation of STAT proteins in T cells distinguishes healthy ageing from unhealthy ageing subjects based on cardiovascular ageing phenotypes17.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [175]
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Metadata
- Authors
- Saleiro, D., & Platanias, L. C.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Platanias, Leonidas C.
- Venue
- Trends in Immunology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 36
- Issue
- 1
- Pages
- 21-29
- ISSN
- 1471-4906 (ISSN-L)
- PMC
- PMC4297313
- OpenAlex
- W2028684481
- Cited by
- 142
- References
- 84
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 10 · 2023: 9 · 2022: 12 · 2021: 17 · 2020: 14 · 2019: 13 · 2018: 12 · 2017: 12 · 2016: 16 · 2015: 7
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA161796, CA-77816, CA121192, R01CA121192, R01CA155566, CA161196, R01CA077816, CA155566, P30CA060553)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- mTOR signaling, STAT signaling, pathway crosstalk, immune cell differentiation, T cells, innate immune cells, immune regulation, immunodeficiency, autoimmunity, signal transduction
- MeSH terms
- Mechanistic Target of Rapamycin Complex 2, Animals, Dendritic Cells, Humans, Immune System, Immunity, Macrophages, Protein Binding, T-Lymphocytes, Signal Transduction, Multiprotein Complexes, STAT Transcription Factors, Receptor, Interferon alpha-beta, TOR Serine-Threonine Kinases
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