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Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

ABSTRACT: Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

PROVIDER: PRJNA562685 | ENA |

REPOSITORIES: ENA

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Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

Project description:Bcl6 play a key role in CD4+ T cell development including follicular regulatory T cells. However, the role of Bcl6 in Treg cells in context of allergic inflammation was not fully understood. In this study, we describe the role of Bcl6 in development and function of ST2+Treg cells by analyzing ST2+Treg cell RNA seq.

2020-04-01 | GSE136556 | GEO

Population gene expression of anti-viral CD4 T cells in Bcl6 and Blimp1 deficient conditions

Project description:Population gene expression of effector CD4+ T cells WT, Bcl6-deficient , Blimp1-deficient or Bcl6 Blimp1-deficient was determined by RNAseq after LCMV Armstrong infection

2021-11-05 | GSE149597 | GEO

Single-cell gene expression of anti-viral CD4 T cells in Bcl6 and Blimp1 deficient conditions

Project description:Single-cell gene expression of effector CD4+ T cells WT, Bcl6-deficient , Blimp1-deficient or Bcl6 Blimp1-deficient was determined by scRNAseq after LCMV Armstrong infection

2021-11-05 | GSE149912 | GEO

Single-cell chromatin accessibility of anti-viral CD4 T cells in Bcl6 and Blimp1 deficient conditions

Project description:Single-cell chromatin accessibility of effector CD4+ T cells WT or Bcl6 Blimp1-deficient was determined by scATACseq after LCMV Armstrong infection

2021-11-05 | GSE149913 | GEO

Dependence on Bcl6 and Blimp1 identifies distinct mechanisms driving memory and follicular helper CD4+ T cell differentiation [scRNA-Seq]

Project description:During the immune response, CD4+ T cells differentiate into distinct effector subtypes, including follicular helper T (Tfh) cells that help B cells, and into memory cells. Tfh and memory cells are required for long-term immunity; both depend on the transcription factor Bcl6, raising the question of whether they differentiate through similar mechanisms. Here, using notably single-cell RNA and ATAC sequencing, we show that virus-responding CD4+ T cells lacking both Bcl6 and Blimp1 can differentiate into cells with transcriptomic, chromatin accessibility and function attributes of memory cells, but not of Tfh cells. Thus, Bcl6 promotes memory cell differentiation primarily through its repression of Blimp1. These findings demonstrate that distinct mechanisms underpin the differentiation of memory and Tfh CD4+ cell and define the Bcl6-Blimp1 axis as a potential target for promoting long-term memory T cell differentiation.

2021-11-14 | GSE184847 | GEO

Dependence on Bcl6 and Blimp1 identifies distinct mechanisms driving memory and follicular helper CD4+ T cell differentiation [scATAC-Seq]

2021-11-14 | GSE184846 | GEO

Bcl6 and Blimp1 reciprocally regulate ST2<sup>+</sup> Treg-cell development in the context of allergic airway inflammation.

Project description:BackgroundBcl6 is required for the development of T follicular helper cells and T follicular regulatory (Tfr) cells that regulate germinal center responses. Bcl6 also affects the function of regulatory T (Treg) cells.ObjectiveThe goal of this study was to define the functions of Bcl6 in Treg cells, including Tfr cells, in the context of allergic airway inflammation.MethodsWe used a model of house dust mite sensitization to challenge wild-type, Bcl6fl/fl Foxp3-Cre, and Prdm1 (Blimp1)fl/fl Foxp3-Cre mice to study the reciprocal roles of Bcl6 and Blimp1 in allergic airway inflammation.ResultsIn the house dust mite model, Tfr cells repress the production of IgE and Bcl6+ Treg cells suppress the generation of type 2 cytokine-producing cells in the lungs. In mice with Bcl6-deficient Treg cells, twice as many ST2+ (IL-33R+) Treg cells develop as are observed in wild-type mice. ST2+ Treg cells in the context of allergic airway inflammation are Blimp1 dependent, express type 2 cytokines, and share features of visceral adipose tissue Treg cells. Bcl6-deficient Treg cells are more susceptible, and Blimp1-deficient Treg cells are resistant, to acquiring the ST2+ Treg-cell phenotype in vitro and in vivo in response to IL-33. Bcl6-deficient ST2+ Treg cells, but not Bcl6-deficient ST2+ conventional T cells, strongly promote allergic airway inflammation when transferred into recipient mice. Lastly, ST2 is required for the exacerbated allergic airway inflammation in Bcl6fl/fl Foxp3-Cre mice.ConclusionsDuring allergic airway inflammation, Bcl6 and Blimp1 play dual roles in regulating Tfr-cell activity in the germinal center and in the development of ST2+ Treg cells that promote type 2 cytokine responses.

| S-EPMC7487006 | biostudies-literature

BLIMP1 controls GC B cell expansion and exit through regulating cell cycle progression and key transcription factors BCL6 and IRF4

Project description:In B cells BLIMP1 is required for plasma cell differentiation. BLIMP1 is also expressed in some dark zone (DZ) germinal center (GC) B cells (GCBCs), yet the role of BLIMP1 in GCBCs is not understood. Here we generated mixed bone marrow (BM) chimeric mice using Prdm1+/+ CD19Cre and Prdm1fl/fl CD19Cre BM, allowing us to examine the cell-intrinsic functions of BLIMP1 in GCBC, independent of antibody or antigen levels. Strikingly, BLIMP1-deficient B cells quickly dominate GCs and persist for a much longer time compared to the wild type cells. BLIMP1 deficiency promotes positive selection of GCBC and enhances cell-cycle progression. In addition, BLIMP1 deficiency enhanced class-switching. Mechanistically, BLIMP1-deficient GCBC fail to downregulate BCL6 and to upregulate IRF4, indicating that BLIMP1 controls the expression of these transcription factors that mediate exit from the GC. These studies revealed unique functions of BLIMP1 in regulating GCBC responses that impact long-lived immune compartments.

2024-03-28 | GSE249811 | GEO

Bcl6 regulates CD8+ T cell fate decision in cancer [RNA-Seq]

Project description:Overcoming CD8+ T cell "exhaustion" is critical in cancer immunotherapy. Intra-tumor CD8+ T cells contain stem-like (Texprog) and terminally differentiated (Texterm) subpopulations that mediate the persistence and potency of anti-tumor responses, respectively. How extrinsic signals via transcription factors control these two subsets are unclear. Previously, Bcl6 was shown to be selectively expressed by Texprog cells and promote their generation in chronic infection. Here, we found that in cancer, Bcl6 deficiency impacted, not the generation, but rather the persistence of Texprog cells, thus abrogating long-term tumor control. Bcl6 expression in CD8+ T cells is reciprocally regulated by TGF-?-SMAD2 and IL-2-STAT5 signaling pathways. Blimp1, regulated by IL-2 signaling, potently inhibited Bcl6 expression and its transcriptional activities; Prdm1 deficiency greatly improved the efficacy of anti-PD-1 therapy. Thus, we identified the TGF-?-Bcl6 and IL-2-Blimp1 antagonistic pathways in regulation of anti-tumor CD8+ T cells, which benefits cancer immunotherapy.

2023-08-15 | GSE182035 | GEO

Bcl6 regulates CD8+ T cell fate decision in cancer [ChIP-Seq]

2023-08-15 | GSE182034 | GEO

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