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The transcription factor BCL6 controls early development of innate-like T cells (ATAC-seq)

ABSTRACT: The transcription factor BCL6 controls early development of innate-like T cells (ATAC-seq)

PROVIDER: PRJNA554325 | ENA |

REPOSITORIES: ENA

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The transcription factor BCL6 controls early development of innate-like T cells (ATAC-seq)

Project description:Innate T cells, including invariant natural killer T (iNKT) and mucosal-associated innate T (MAIT) cells, are a heterogeneous T lymphocyte population with effector properties pre-programmed during their thymic differentiation. How this program is initiated is currently unclear. Here, we show that the transcription factor BCL6 is transiently expressed in iNKT cells upon exit from positive selection and is required for their proper development beyond stage 0. Notably, development of MAIT cells is also impaired in Bcl6-deficient mice. We found that BCL6 regulates the expression of genes that are associated with the innate T cell lineage, including PLZF and its targets. BCL6 contributes to a chromatin accessibility landscape that is permissive for the expression of development-related genes and inhibitory for genes associated with naïve T cell programs. Our results reveal novel functions for BCL6 and indicate that this transcription factor controls the inception of innate T cell lineage programming.

2020-07-27 | GSE134210 | GEO

The transcription factor BCL6 controls early development of innate-like T cells (RNA-seq)

2021-07-03 | GSE134211 | GEO

The transcription factor BCL6 controls early development of innate-like T cells

Project description:The transcription factor BCL6 controls early development of innate-like T cells

| PRJNA554319 | ENA

The transcription factor BCL6 controls early development of innate-like T cells (RNA-seq)

Project description:The transcription factor BCL6 controls early development of innate-like T cells (RNA-seq)

| PRJNA554324 | ENA

Single-cell RNAseq of murine Bcl6-deficient ILC against wild-type controls

Project description:Innate lymphoid cells (ILC) are tissue-resident effector cells with important roles in tissue homeostasis, protective immunity and inflammatory disease. Here we investigated the role of the transcription factor Bcl6 in small intestinal innate lymphoid cells. Specifically, we performed single-cell RNA-seq on total small intestine lamina propria ILCs from tamoxifen-treated Id2-CreERT2 ROSA26-tdRFP Bcl6-fl/fl mice and Id2-CreERT2 ROSA26-tdRFP controls.

2023-10-31 | E-MTAB-12864 | biostudies-arrayexpress

Bcl6 mediates innate immune response

Project description:Using microarrays, we compared the changes in levels of gene expression between wildtype and Bcl6 KO macrophages in the absence or presence of LPS. Total RNA was obtained from WT and Bcl6 KO unstimulated and LPS-stimulated primary bone marrow-derived macrophages

2010-11-24 | E-GEOD-24792 | biostudies-arrayexpress

Bcl6 mediates innate immune response

Project description:Using microarrays, we compared the changes in levels of gene expression between wildtype and Bcl6 KO macrophages in the absence or presence of LPS.

2010-11-24 | GSE24792 | GEO

The transcription factor BCL6 controls early development of innate-like T cells

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

2020-07-27 | GSE134212 | GEO

Cell autonomous expression of Bcl6 is required to maintain lineage identity of mouse CCR6+ ILC3s

Project description:Innate lymphoid cells (ILC) are similar to T helper (Th) cells in expression of cytokines and transcription factors. For example, RORγt is the lineage-specific transcription factor for both ILC3 and Th17 cells. However, the ILC counterpart for BCL6-expressing T follicular helper (Tfh) cells has not been defined. Here, we report that in the ILC compartment, BCL6 is selectively co-expressed with not only CXCR5, but also RORγt and CCR6 in ILC3 from multiple tissues. BCL6-deficient ILC3 produce enhanced levels of IL-17A and IL-22. More importantly, phenotypic and single-cell ATAC-seq analysis show that absence of BCL6 in mature ILC3 increases the numbers of ILC1 and transitional cells co-expressing ILC3 and ILC1 marker genes. A lineage-tracing experiment further reveals BCL6+ ILC3 to ILC1 trans-differentiation under steady state. Lastly, microbiota promote BCL6 expression in colonic CCR6+ ILC3, and thus reinforce their stability. Collectively, our data have demonstrated that CCR6+ ILC3 have both Th17 and Tfh programs and that BCL6 expression in these cells functions to maintain their lineage identity.

2022-12-27 | GSE221341 | GEO

A Bcl6-Smrt/Ncor repression program controls atherosclerosis

Project description:This SuperSeries is composed of the following subset Series: GSE27001: Inhibition of Bcl6-SMRT/NCoR interactions by an inhibitory peptide affects inflammatory pathways GSE27033: Genome-wide location analysis of SMRT and NCoR in wild-type and Bcl6 knockout macrophages Refer to individual Series

2012-03-29 | E-GEOD-27060 | biostudies-arrayexpress

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