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Treg cells and Treg-specific deletion of Blimp1

ABSTRACT: Treg cells and Treg-specific deletion of Blimp1

PROVIDER: PRJNA737436 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14807704_1.fastq.gz	Fastqsanger.gz
	SRR14807704_2.fastq.gz	Fastqsanger.gz
	SRR14807705_1.fastq.gz	Fastqsanger.gz
	SRR14807705_2.fastq.gz	Fastqsanger.gz
	SRR14807706_1.fastq.gz	Fastqsanger.gz

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Gene analysis of tumor cells from mice with the Treg-specific deletion of Blimp1 compared to WT mice (NanoString Cancer)

Project description:We observed that mice with the Treg-specific deletion of Blimp1 had delayed and smaller tumor growth associated with the activation of tumor-infiltrating immune effector cells. To determine what extent disruptions of Treg suppressive activity by a specific deletion of Blimp1 could impact on the tumor, we assessed the gene expression of sorted tumor cells by NanoString analysis.

2021-11-24 | GSE178134 | GEO

Gene analysis of tumor cells from mice with the Treg-specific deletion of Blimp1 compared to WT mice (NanoString Immune)

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Gene expression profiles of mouse Blimp1 +/gfp and Blimp1 gfp/gfp regulatory T cells

Project description:Regulatory T (Treg) cells are required for peripheral tolerance. Recent evidence indicates that Treg cells can adopt specialized differentiation programs in the periphery that are controlled by transcription factors usually associated with T helper differentiation. We demonstrate that expression of the transcription factor Blimp1 defines a population of Treg cells that localize predominantly to mucosal sites and produces IL-10. Blimp1 is required for IL-10 production by these cells and for their tissue homeostasis. A list of differentially expressed genes were identified from this whole-genome expression profiling experiment. Mouse Blimp1 +/gfp and Blimp1 gfp/gfp regulatory T cells were analyzed. Three replicates each.

2011-02-09 | E-GEOD-27143 | biostudies-arrayexpress

Gene analysis of tumor cells from mice with the Treg-specific deletion of Blimp1 compared to WT mice (NanoString Immune)

Project description:Gene analysis of tumor cells from mice with the Treg-specific deletion of Blimp1 compared to WT mice (NanoString Immune)

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Project description:Gene analysis of tumor cells from mice with the Treg-specific deletion of Blimp1 compared to WT mice (NanoString Cancer)

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Gene expression profiles of mouse Blimp1 +/gfp and Blimp1 gfp/gfp regulatory T cells

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HDAC10 deletion in Treg

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Blimp1 is required to repress Foxp3+ regulatory T cell pathogenic activity in mice

Project description:Foxp3+Tregcells are essential modulators of immune responses but under specific conditions can acquire inflammatory properties and potentially contribute to disease pathogenesis. Here we show that the transcription factor Blimp1 is a critical regulator of Foxp3+Treg functional plasticity. The intrinsic expression of Blimp1 was required to prevent Treg from producing Th17-associated cytokines and acquiring an inflammatory phenotype while preserving Foxp3 expression. Mechanistically, Blimp1 acts as a direct repressor of the Il17a/Il17f genes in Foxp3+Treg and binding of Blimp1 at this locus is associated with altered chromatin status, reduced binding the co-activator p300, unaltered binding of the Th17-asssociated transcription factor RORt and more abundant binding of IRF4, which was required for the production of IL17A in Blimp1-deficient Foxp3+Tregcells, as shown by IRF4 siRNA-mediated knockdown. Consistent with their capacity to produce inflammatory cytokines, Blimp1-deficient Foxp3+Treg exacerbate Th17-mediated inflammation in vivo indicating that Blimp1 is required to prevent Treg cells from acquiring pathogenic properties

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Blimp1 maintains regulatory T cell identity at sites of inflammation through epigenetic imprinting

Project description:Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. We here establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway was dependent on the transcriptional regulator Blimp1, which prevented dismantling of Foxp3 expression and "toxic" gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulated IL-6- and STAT3-mediated methylation of Treg cell-specific conserved non-coding sequence 2 (CNS2) in the Foxp3 locus. Consequently, CNS2 was heavily methylated when Blimp1 was ablated, leading to loss of Foxp3 expression and severe disease. These findings identify a Blimp1-dependent epigenetic pathway that preserves Treg cell stability in inflamed non-lymphoid tissues.

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