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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

ABSTRACT: In order to investigate whether Bcl11b mediates any chormatin accebility in Treg cell, we performed ATAC-Seq from Bcl11b sufficient (WT) and Bcl11b deficient Treg(KO) cells.We used 100,000 cells for each experiment.

ORGANISM(S): Mus musculus

PROVIDER: GSE130059 | GEO | 2019/08/07

REPOSITORIES: GEO

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

Project description:In order to identify Bcl11b-bound sites in Treg cells(WT) and Tn cells and to determine Bcl11n and Foxp3 peak overlaps, we performed Bcl11b and Foxp3 ChIP-seq on respective cell populations. In order to understand whether Bcl11b recruitment to it's target sites is dependent on Foxp3 we performed Bcl111b ChIP-Seq in Tfn cells(derived from Foxp3GFPKO mice). Finally, to ask whether genome-wide occupancy of Foxp3 is affected in the absence of Bcl11b, we performed Foxp3 ChIP-seq in Bcl11b-deficient Treg cells(KO Treg).

2019-08-07 | GSE120947 | GEO

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

Project description:In order to acquire in depth understanding of Treg specific molecular functions of Bcl11b, we performed RNA-Seq from Bcl11b-suffcient or deficient Treg cells to determine transcriptional profile.

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of a regulatory T cell gene expression program.

Project description:Foxp3 and its protein partners establish a regulatory T (Treg) cell transcription profile and promote immunological tolerance. However, molecular features contributing to a Treg-specific gene expression program are still incompletely understood. We find that the transcription factor Bcl11b is a prominent Foxp3 cofactor with multifaceted functions in Treg biology. Optimal genomic recruitment of Foxp3 and Bcl11b is critically interdependent. Genome-wide occupancy studies coupled with gene expression profiling reveal that Bcl11b, in association with Foxp3, is primarily responsible in establishing a Treg-specific gene activation program. Furthermore, Bcl11b restricts misdirected recruitment of Foxp3 to sites, which would otherwise result in an altered Treg transcriptome profile. Consequently, Treg-specific ablation of Bcl11b results in marked breakdown of immune tolerance, leading to aggressive systemic autoimmunity. Our study provides previously underappreciated mechanistic insights into molecular events contributing to basic aspects of Treg function. Furthermore, it establishes a therapeutic target with potential implications in autoimmunity and cancer.

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

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

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

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Tregs from Bcl11b-deficient versus wild type Tregs (CD4Cre and Foxp3Cre systems)

Project description:expression profile in Bcl11b-deficient Treg cells versus wild type Treg cells Treg cells sorted from Bcl11bF/F/Cd4Cre/Foxp3-GFP+ mice and wild type Foxp3-GFP+ mice Treg cells sorted from Bcl11bF/F/Foxp3Cre mice and wild type mice RNA extracted from sorted Bcl11b-deficient Foxp3-GFP Treg cells form Bcl11bF/F/Cd4Cre/Foxp3-GFP+ mice and wild type Foxp3-GFP Treg cells; expression profile by microarray analysis RNA extracted from sorted Bcl11b-deficient Treg cells form Bcl11bF/F/Foxp3Cre mice and wild type Treg cells; expression profile by microarray analysis

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

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Mapping Bcl11b binding in regulatory T cells

Project description:T regulatory (Treg) cells have been studied in depth since their discovery for their potential use in therapies of autoimmune diseases. Treg cells have a suppression program that includes surface molecules CD25 (IL2R), cytotoxic T-lymphocyte associated protein 4 (CTLA4), and glucocorticoid-induced TNFR family (GITR) to limit aberrant and excessive inflammatory immune responses. We have shown that Bcl11b can bind to the CNS2 region in Foxp3 as well as the gene loci of those essential surface molecules for Treg suppression. Furthermore, we have identified a subset of Foxp3-independent genes in Treg cells directly regulated by Bcl11b binding. Bcl11b also directly represses expression of innate molecules such as transcription factors PU.1 and ID2 in Treg cells. Finally, we have also shown that removal of Bcl11b accelerates apoptosis in Treg cells as cleaved caspase 3 levels were significantly elevated in Bcl11b KO Treg cells when compared with WT Treg cells.

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