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Single cell transcriptomic analysis (10x Genomics) of mouse colon LP CD4+ Tcells cells isolated from mouse under different infection conditions [bulk RNA]

ABSTRACT: To determine the states that Teff actually adopt in frontline tissues in vivo, we applied single-cell transcriptome and chromatin analysis on colonic Teff cells, in germ-free or conventional mice, or after challenge with a range of Teff subset-biasing microbes. Subsets were marked by expression of interferon-signature or myeloid-specific transcripts, but transcriptome or chromatin structure could not resolve discrete Th clusters. At baseline or at different times of infection, transcripts encoding cytokines or proteins commonly used as Teff markers distributed in a polarized continuum, which was also functionally validated. Clones derived from single progenitors gave rise to both IFN-γ and IL17-producing cells. Most transcriptional variance was tied to the infecting agent, independent of the cytokines produced, and chromatin variance primarily reflected activity of AP1 and IRF transcription factor families, not the canonical subset master regulators T-bet, GATA3, RORγ.

ORGANISM(S): Mus musculus

PROVIDER: GSE160054 | GEO | 2020/12/31

REPOSITORIES: GEO

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Single cell transcriptomic analysis (10x Genomics) of mouse colon LP CD4+ Tcells cells isolated from mouse under different infection conditions

Project description:To determine the states that Teff actually adopt in frontline tissues in vivo, we applied single-cell transcriptome and chromatin analysis on colonic Teff cells, in germ-free or conventional mice, or after challenge with a range of Teff subset-biasing microbes. Subsets were marked by expression of interferon-signature or myeloid-specific transcripts, but transcriptome or chromatin structure could not resolve discrete Th clusters. At baseline or at different times of infection, transcripts encoding cytokines or proteins commonly used as Teff markers distributed in a polarized continuum, which was also functionally validated. Clones derived from single progenitors gave rise to both IFN-γ and IL17-producing cells. Most transcriptional variance was tied to the infecting agent, independent of the cytokines produced, and chromatin variance primarily reflected activity of AP1 and IRF transcription factor families, not the canonical subset master regulators T-bet, GATA3, RORγ.

2020-12-31 | GSE160053 | GEO

Regulatory T cells from colonic lamina propria [array]

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2015-07-25 | E-GEOD-68009 | biostudies-arrayexpress

Alternative activation of mast cells by CD4+ T helper cells

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Regulatory T cells from colonic lamina propria [RNA-Seq]

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Translation Control in CD4 T Cell Activation enforced by T-regulatory cells

Project description:Increased protein synthesis is a hallmark of CD4 effector T cell (Teff) activation. Regulatory T cells (Tregs) suppress the activation, proliferation, and subsequent effector functions of Teff cells. Several mechanisms have been proposed for Treg-mediated suppression, including release of suppressive cytokines and expression of inhibitory receptors. However, molecular mechanisms that enforce suppression on Teff cell function are unclear. Control of CD4 effector T cell activation has largely been defined at the transcriptional level, which does not reflect changes in post-transcriptional control. We Tregs suppress CD4 Teff activation through regulation of global protein synthesis prior to cell division. Using polysome profiling, we analyzed genome-wide changes in the transcriptome and translatome of activated CD4 Teff cells. We found that mRNAs encoding for the protein synthesis machinery are regulated at the level of translation in activated Teff cells, and that Tregs their translation without affecting their transcription. This translational inhibition is controlled by Treg-mediated regulation of Torc1 signaling. These data show that peripheral tolerance is enforced by Tregs through mRNA translational control in Teff cells.

2022-01-20 | GSE171789 | GEO

Nuclear receptor RORγ is a targetable master regulator of cholesterol in a subtype of breast cancer [RNA-Seq]

Project description:We show that triple-negative breast cancer (TNBC) exhibits a hyper-activated MVA-CB program that is strongly linked to nuclear receptor RORγ, compared to estrogen receptor-positive breast cancer. Genetic and pharmacological inhibition of RORγ reduces tumor cholesterol contents and synthesis rate while preserving host cholesterol homeostasis. We demonstrate, for the first time, that RORγ functions as a master activator of the entire MVA-CB program, dominantly over SREBP2, through its own direct binding and facilitating the recruitment of SREBP2. RORγ inhibition disrupts its association with SREBP2 and reduces MVA-CB chromatin acetylation. RORγ antagonists cause sustained TNBC tumor regression in patient-derived and immune-intact models. Their combination with cholesterol-lowering statins elicits superior anti-tumor synergy selectively in TNBC. Together, our studies uncover a previously unsuspected master regulator of MVA-CB and an attractive target for TNBC.

2019-08-04 | GSE131856 | GEO

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Expression data from Human CD40L+ Tcells

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