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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE178133 | GEO | 2021/11/24

REPOSITORIES: GEO

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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

Treg cells and Treg-specific deletion of Blimp1

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

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

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.

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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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Gene expression profile of effector Treg cells isolated from spleens and tumors of tumor-bearing mice

Project description:A majority of effector Treg cells (eTregs) that are abundant in many types of tumors are marked by the expression of Blimp1. However, the specific impact of Blimp1+ eTregs on, and mechanisms of action within, tumors remain unknown. To better understand the role of Blimp1 in the regulation of eTreg function in the tumor immunity, we profiled the differential gene expression in Blimp1-deficient eTregs compared to WT control eTregs from tumor-bearing mice.

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

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RNA-seq analysis of transcriptomes of IL35-Treg cells and the Blimp1-Treg cells

Project description:To gain in depth transcriptional information about the two subsets of effector Tregs, we performed RNA-seq analysis to compare the transcriptomes of Thy1.1+Blimp1- (Ebi3-Tregs) and Thy1.1-Blimp1+ (Blimp1-Tregs) Tregs. We found ~173 unique genes with differential expression between the two effector subsets.

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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.

2018-10-26 | GSE121764 | GEO

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