Regulation of Immune Responses by mTOR

Powell, Jonathan D.; Pollizzi, Kristen N.; Heikamp, Emily B.; Horton, Maureen R.

doi:10.1146/annurev-immunol-020711-075024

Cited by 836PI3K/AKT/mTOR signaling in cancerT-cell and B-cell ImmunologySignaling Pathways in Disease

Regulation of Immune Responses by mTOR

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Powell, Jonathan D., Pollizzi, Kristen N., Heikamp, Emily B., Horton, Maureen R.·2012·Annual Review of Immunology

DOI 10.1146/annurev-immunol-020711-075024PMC PMC3616892

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Abstract

mTOR is an evolutionarily conserved serine/threonine kinase that plays a central role in integrating environmental cues in the form of growth factors, amino acids, and energy. In the study of the immune system, mTOR is emerging as a critical regulator of immune function because of its role in sensing and integrating cues from the immune microenvironment. With the greater appreciation of cellular metabolism as an important regulator of immune cell function, mTOR is proving to be a vital link between immune function and metabolism. In this review, we discuss the ability of mTOR to direct the adaptive immune response. Specifically, we focus on the role of mTOR in promoting differentiation, activation, and function in T cells, B cells, and antigen-presenting cells.

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Crossref · 10.1146/annurev-immunol-020711-075024

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The activation of inflammatory and growth factor regulators in the subiculum indicates convergence of mTOR/INS dysregulation with neuroimmune and receptor tyrosine kinase signaling in DS-AD.
“Upstream regulator analysis based on the proteome identified strong activation of inflammatory and growth factor regulators, including TGFB1, TNF, EGFR, and ERBB2, particularly in the subiculum, indicating convergence of mTOR/INS dysregulation with neuroimmune and receptor tyrosine kinase signaling in DS‐AD, 65 which warrants further investigation.”
From Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations (2026) · cites this paper as [65]
The ‘Upstream Regulation of mTOR Activity’ section says that cytokine and growth-factor receptors can activate mTOR, supporting a general connection between immune and growth-factor signaling. It does not report a subiculum proteomic analysis, activation of TGFB1, TNF, EGFR, or ERBB2, or convergence of these pathways in DS-AD. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Upstream regulator analysis based on the proteome identified strong activation of inflammatory and growth factor regulators, including TGFB1, TNF, EGFR, and ERBB2, particularly in the subiculum.
“Upstream regulator analysis based on the proteome identified strong activation of inflammatory and growth factor regulators, including TGFB1, TNF, EGFR, and ERBB2, particularly in the subiculum, indicating convergence of mTOR/INS dysregulation with neuroimmune and receptor tyrosine kinase signaling in DS‐AD, 65 which warrants further investigation.”
From Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations (2026) · cites this paper as [65]
The review’s “Upstream Regulation of mTOR Activity” section discusses growth-factor and immune signaling that regulates mTOR, but does not report a proteome-based upstream regulator analysis. Searches for the named regulators, subiculum, and DS-AD found no passage addressing their claimed activation. (LLM, conf=0.76)
Experimental — accuracy not yet measured
IGF-1, released by microglia and able to lessen some behavioral and neuropathological features of Rett and 22q13 deletion syndrome, turns on mTOR.
“IGF-1, which ameliorates some behavioural and neuropathologies of Rett and 22q13 deletion syndrome, and is secreted by microglia, activates mTOR230.”
From Immune mediators in the brain and peripheral tissues in autism spectrum disorder (2015) · cites this paper as [230]
The lack of mitochondrial biogenesis in senescent T cells may be a consequence of the failure of these cells to activate mTOR, as demonstrated by their inability to phosphorylate mTORC1 or mTORC2.
“The lack of mitochondrial biogenesis may well be a consequence of the failure of senescent T cells to activate mTOR (mammaliam target of rapamycin), a central integrator of immune signalling and cell metabolism [62], as demonstrated by their inability to phosphorylate the mTOCR1 [25] or the mTORC2 complex [63].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [62]

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Authors: Powell, J. D., Pollizzi, K. N., Heikamp, E. B., & Horton, M. R.
Affiliations: Sidney Kimmel Cancer Center (US)
Johns Hopkins University (US)
Corresponding author: Pollizzi, Kristen N.
Heikamp, Emily B.
ORCID: Powell, Jonathan D.
Heikamp, Emily B.
Horton, Maureen R.
Venue: Annual Review of Immunology
Publisher: Annual Reviews
Published: 2012-04-23
Volume: 30
Issue: 1
Pages: 39-68
ISSN: 0732-0582 (ISSN-L)
1545-3278
DOI: 10.1146/annurev-immunol-020711-075024
PMC: PMC3616892
OpenAlex: W2164917731
Cited by: 836
References: 171
Citations by year: 2026: 46 · 2025: 40 · 2024: 56 · 2023: 59 · 2022: 53 · 2021: 73 · 2020: 65 · 2019: 70 · 2018: 58 · 2017: 65 · 2016: 67 · 2015: 76 · 2014: 47 · 2013: 47 · 2012: 14
FWCI: 5.37
Type: journal article
Language: en
Open access: green
europepmc.org
Locations: Annual Review of Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Heart, Lung, and Blood Institute (R21HL111783, R01HL073855)
National Cancer Institute (P30CA006973)
National Institute of Allergy and Infectious Diseases (R01AI077610, R01AI091481, T32AI007247)
Topics: 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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords: mTOR, immune regulation, cellular metabolism, T cell differentiation, B cell activation, antigen-presenting cells, adaptive immune response, immune microenvironment, amino acid sensing, energy sensing, growth factor signaling
MeSH terms: Animals, Antigen-Presenting Cells, B-Lymphocytes, Cell Differentiation, Enzyme Activation, Humans, Immunity, Immunosuppressive Agents, Lymphocyte Activation, T-Lymphocytes, Signal Transduction, Protein Kinase Inhibitors, T-Lymphocytes, Regulatory, TOR Serine-Threonine Kinases

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Regulation of Immune Responses by mTOR

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