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

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

PROVIDER: PRJNA766646 | ENA |

REPOSITORIES: ENA

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

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

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Dependence on Bcl6 and Blimp1 identifies distinct mechanisms driving memory and follicular helper CD4+ T cell differentiation

Project description:Dependence on Bcl6 and Blimp1 identifies distinct mechanisms driving memory and follicular helper CD4+ T cell differentiation

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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

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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

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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.

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Dependence on Bcl6 and Blimp1 drive distinct differentiation of murine memory and follicular helper CD4+ T cells.

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 whether they differentiate through similar mechanisms. Here, using 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 functional 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+ cells and define the Bcl6-Blimp1 axis as a potential target for promoting long-term memory T cell differentiation.

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Dependence on Bcl6 and Blimp1 identifies distinct mechanisms driving memory and follicular helper CD4+ T cell differentiation

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

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