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Deconstructive SCNT reveals heterogeneity within Treg population [single-cell]

ABSTRACT: Thymic-derived Treg cells consist of heterogeneous subsets with different characteristics and development.

ORGANISM(S): Mus musculus

PROVIDER: GSE97849 | GEO | 2018/05/30

REPOSITORIES: GEO

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Deconstructive SCNT reveals heterogeneity within Treg population [bulk]

Project description:Thymic-derived Treg cells consist of heterogeneous subsets with different characteristics and development.

2018-05-30 | GSE97848 | GEO

Deconstructive SCNT reveals heterogeneity within Treg population

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Deconstructive SCNT reveals heterogeneity within Treg population

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DRAK2 alters IL-2 sensitivity and Treg development

Project description:Drak2¬-deficient (Drak2-/-) mice are resistant to multiple models of autoimmunity, yet effectively eliminate pathogens and tumors. Thus, DRAK2 is an ideal target to treat autoimmune diseases. However, the mechanisms by which DRAK2 contributes to autoimmunity, particularly type 1 diabetes (T1D), remain unresolved. Our data indicate that DRAK2 contributes to autoimmunity in multiple ways by regulating thymic Treg development and by impacting the sensitivity of conventional T cells to Treg-mediated suppression.

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Project description:Regulatory T (Treg) cells derived from the thymus (tTreg) and periphery (pTreg) play central and distinct roles in immunosuppression, but mechanisms governing the generation and activation of Treg subsets in vivo remain uncertain. Here, we report that mechanistic target of rapamycin (mTOR) unexpectedly supports the homeostasis and functional activation of tTreg and pTreg cells. Further, mTOR signaling is crucial for programming activated Treg cell effector function to protect immune tolerance and tissue homeostasis. Treg-specific deletion of mTOR drives spontaneous TH2 responses and altered barrier tissue homeostasis, associated with reductions in both thymic derived effector Treg (eTreg) and pTreg cells. Mechanistically, mTOR acts downstream of antigenic signals to drive IRF4 expression and mitochondrial metabolism, and accordingly, disruption of mitochondrial metabolism severely impairs Treg cell suppressive function and their homeostasis in tissues. Collectively, our results demonstrate that mTOR coordinates transcriptional and metabolic programs in activated Treg subsets to mediate tissue homeostasis

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