Evidence map›Paper›PMID 28600802›Full record

ReviewFEBS letters2017

mTORC1 and mTORC2 as regulators of cell metabolism in immunity.

Monika Linke, Stephanie Deborah Fritsch, Nyamdelger Sukhbaatar, Markus Hengstschläger, Thomas Weichhart

Open access · bronzeAbstract readReview
In one paragraph

Review in FEBS letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

160 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The authors respond to feedback onFrontiers in oncology · 2026
    Article
  14. Polyploidy and Senescence of Cancer Cells: Impact of Cell Fusion.Advances in experimental medicine and biology · 2026
    Review
  15. Article
  16. Propagation of monocyte exhaustion memory and underlying mechanisms.Cell communication and signaling : CCS · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. Review

100 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Monika LinkeCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.
Stephanie Deborah FritschCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.
Nyamdelger SukhbaatarCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.
Markus HengstschlägerCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.
Thomas WeichhartCenter of Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical University of Vienna, Austria.ORCID 0000-0002-4349-0797
Medical University of Vienna · AT

Funding

Austrian Science Fund FWF P 27701Austrian Science Fund FWF P 30857
6 · The paper itself

Abstract

The mechanistic target of rapamycin (mTOR) pathway is an evolutionarily conserved signaling pathway that senses intra- and extracellular nutrients, growth factors, and pathogen-associated molecular patterns to regulate the function of innate and adaptive immune cell populations. In this review, we focus on the role of the mTOR complex 1 (mTORC1) and mTORC2 in the regulation of the cellular energy metabolism of these immune cells to regulate and support immune responses. In this regard, mTORC1 and mTORC2 generally promote an anabolic response by stimulating protein synthesis, glycolysis, mitochondrial functions, and lipid synthesis to influence proliferation and survival, effector and memory responses, innate training and tolerance as well as hematopoietic stem cell maintenance and differentiation. Deactivation of mTOR restores cell homeostasis after immune activation and optimizes antigen presentation and memory T-cell generation. These findings show that the mTOR pathway integrates spatiotemporal information of the environmental and cellular energy status by regulating cellular metabolic responses to guide immune cell activation. Elucidation of the metabolic control mechanisms of immune responses will help to generate a systemic understanding of the immune system.

Indexed as

ImmunityAnimalsCellsHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MitochondriaModels, BiologicalMultiprotein ComplexesTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Multiprotein ComplexesTOR Serine-Threonine Kinasesdendritic cellglycolysisimmune cell metabolismlipid metabolismmacrophagemitochondriamTORC1mTORC2T-cell

Identifiers

PMID28600802
PMCPMC6322652
OpenAlexW2622166486

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.