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mTOR coordinates transcriptional programs and mitochondrial metabolism of activated Treg subsets to protect tissue homeostasis
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mTOR coordinates transcriptional programs and mitochondrial metabolism of activated Treg subsets to protect tissue homeostasis
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Journal Article
mTOR coordinates transcriptional programs and mitochondrial metabolism of activated Treg subsets to protect tissue homeostasis
2018
Overview
Regulatory T (T
reg
) cells derived from the thymus (tT
reg
) and periphery (pT
reg
) have central and distinct functions in immunosuppression, but mechanisms for the generation and activation of T
reg
subsets in vivo are unclear. Here, we show that mechanistic target of rapamycin (mTOR) unexpectedly supports the homeostasis and functional activation of tT
reg
and pT
reg
cells. mTOR signaling is crucial for programming activated T
reg
-cell function to protect immune tolerance and tissue homeostasis. T
reg
-specific deletion of mTOR drives spontaneous effector T-cell activation and inflammation in barrier tissues and is associated with reduction in both thymic-derived effector T
reg
(eT
reg
) and pT
reg
cells. Mechanistically, mTOR functions downstream of antigenic signals to drive IRF4 expression and mitochondrial metabolism, and accordingly, deletion of mitochondrial transcription factor A (Tfam) severely impairs T
reg
-cell suppressive function and eT
reg
-cell generation. Collectively, our results show that mTOR coordinates transcriptional and metabolic programs in activated T
reg
subsets to mediate tissue homeostasis.
The authors previously showed that mTOR controls the function of regulatory T cells. Here they show how this mTOR signaling orchestrates homeostasis of T
reg
-cell subsets and prevents fatal autoimmunity.
