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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

ABSTRACT: Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

PROVIDER: PRJNA645367 | ENA |

REPOSITORIES: ENA

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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases

Project description:Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases

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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [FFoxp3-GFP-hCre]

Project description:Upregulate and stabilize Foxp3 expression in Treg are essential for manipulating Treg cell function and immune homeostasis. Here, we examined the potential role and mechanism of gp96 protein in regulating FoxP3 transcription and Treg activation in vivo.

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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [Foxp3Cre Myd88fl/fl]

Project description:Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases [Foxp3Cre Myd88fl/fl]

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Heat shock protein gp96 induces Foxp3 expression in Regulatory T Cells via interaction with TLRs for treatment of Auto-immune Diseases

Project description:This SuperSeries is composed of the SubSeries listed below.

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Dominant Th2 differentiation of human regulatory T cells upon loss of FOXP3 expression

Project description:CD4+CD25+FOXP3+ regulatory T cells (Treg) are pivotal for peripheral self-tolerance. They prevent immune responses to auto- and alloantigens and are thus under close scrutiny as cellular therapeutics for autoimmune diseases and the prevention or treatment of alloresponses after organ or stem cell transplantation. We previously showed that human Treg cells with a memory cell phenotype, but not those with a naïve phenotype, rapidly down-regulate expression of the lineage-defining transcription factor forkhead box P3 (FOXP3) upon in vitro expansion. We now compared the transcriptomes of stable FOXP3+ Treg and converted FOXP3- 'ex-Treg' cells by applying a newly developed intranuclear staining protocol that permits the isolation of intact mRNA from fixed, permeabilized and FACS-purified cell populations. Whole genome microarray analysis revealed strong and selective upregulation of Th2 signature genes, including GATA-3, IL-4, IL-5 and IL-13, upon downregulation of FOXP3. Th2 differentiation of converted, FOXP3- ex-Treg cells occurred even under non-polarizing conditions and could not be prevented by IL-4 signaling blockade. Thus, our studies identify Th2 differentiation as the default developmental program of human Treg cells after downregulation of FOXP3. RNA preparations from FOXP3 stained in vitro expanded CD4+CD25highCD45RA- “memory” Treg cells from five independent donors were analyzed using Whole Human Genome Oligo Microarrays (Agilent). An adapted FOXP3 staining procedure to stain FOXP3 in human regulatory T cells to isolate intact RNA for microarray hybridization was developed (see extract protocol).

2011-12-14 | E-GEOD-26190 | biostudies-arrayexpress

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Project description:IL-34 deficiency impairs FOXP3+ Treg function and increases susceptibility to diseases

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Expression Data of Treg and Tconv Cells from FoxP3-GFP Chimeric and FoxP3-ires-GFP B6 and NOD Mice

Project description:The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program.

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