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Current Opinion in Cell Biology
Article . 2011 . Peer-reviewed
License: Elsevier TDM
Data sources: Crossref
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TOR in the immune system

Authors: Koichi, Araki; Ali H, Ellebedy; Rafi, Ahmed;

TOR in the immune system

Abstract

The target of rapamycin (TOR) is a crucial intracellular regulator of the immune system. Recent studies have suggested that immunosuppression by TOR inhibition may be mediated by modulating differentiation of both effector and regulatory CD4 T cell subsets. However, it was paradoxically shown that inhibiting TOR signaling has immunostimulatory effects on the generation of long-lived memory CD8 T cells. Beneficial effects of TOR inhibition have also been observed with dendritic cells and hematopoietic stem cells. This immune modulation may contribute to lifespan extension seen in mice with mTOR inhibition. Here, we review recent findings on TOR modulation of innate and adaptive immune responses, and discuss potential applications of regulating TOR to provide longer and healthier immunity.

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Keywords

CD4-Positive T-Lymphocytes, TOR Serine-Threonine Kinases, Cell Differentiation, Dendritic Cells, Adaptive Immunity, Immunity, Innate, T-Lymphocyte Subsets, Animals, Humans, Signal Transduction

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    121
    popularity
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    Top 10%
    influence
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
121
Top 10%
Top 10%
Top 1%
bronze