The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment
What this study shows
T cells lacking mTOR fail to become normal effector cells and default toward regulatory T cells, showing mTOR is a master switch for immune cell fate.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Mouse (T cells)) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Mouse (T cells) |
| Journal | Immunity |
| Year | 2009 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.immuni.2009.04.014 · PMID 19538929 · Free full text (PMC2768135) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Genetic (mTOR-deficient T cells) |
| Target | mTOR |
| Model | Mouse (T cells) |
| Effect | mTOR is required for effector T-cell differentiation; its loss biases cells toward the regulatory T-cell lineage |
In the Atlas
Related topics
More studies on this topic
- The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2 (2011)
- mTORC1 and mTORC2 selectively regulate CD8+ T cell differentiation (2015)
- The role of mTORC2/RICTOR in immune cells and inflammatory diseases. (2026)
- Regulation and function of mTOR signalling in T cell fate decisions (2012)
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