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Genome-wide DNA methylation landscape defines specialization of regulatory T cells in tissues

ABSTRACT: Genome-wide DNA methylation landscape defines specialization of regulatory T cells in tissues

PROVIDER: PRJEB14591 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1518900_1.fastq.gz	Fastqsanger.gz
	ERR1518900_2.fastq.gz	Fastqsanger.gz
	ERR1518891_1.fastq.gz	Fastqsanger.gz
	ERR1518891_2.fastq.gz	Fastqsanger.gz
	ERR1518901_1.fastq.gz	Fastqsanger.gz

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Genome-wide DNA-methylation landscape defines specialization of regulatory T cells in tissues.

Project description:Regulatory T cells (Treg cells) perform two distinct functions: they maintain self-tolerance, and they support organ homeostasis by differentiating into specialized tissue Treg cells. We found that epigenetic modifications defined the molecular characteristics of tissue Treg cells. Tagmentation-based whole-genome bisulfite sequencing revealed more than 11,000 regions that were methylated differentially in pairwise comparisons of tissue Treg cell populations and lymphoid T cells. Similarities in the epigenetic landscape led to the identification of a common tissue Treg cell population that was present in many organs and was characterized by gain and loss of DNA methylation that included many gene sites associated with the TH2 subset of helper T cells, such as the gene encoding cytokine IL-33 receptor ST2, as well as the production of tissue-regenerative factors. Furthermore, the ST2-expressing population was dependent on the transcriptional regulator BATF and could be expanded by IL-33. Thus, tissue Treg cells integrate multiple waves of epigenetic reprogramming that define their tissue-restricted specialization.

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Cognate antigen recognition defines intestinal Treg specialization and stability

Project description:Regulatory CD4 T cells (Treg) confer non-overlapping functions in intestinal immune tolerance, tissue maintenance, repair, and regeneration. Cytokines and T cell receptor (TCR) signals, in combination with environmental cues, direct Treg proliferation and differentiation. However, how intestinal antigens shape intestinal Treg populations, their specialization and stability remain unknown. Here we show that only Treg bearing specific TCRs expand in the colon, resulting in highly oligoclonal Treg populations. Treg TCR repertoires are private, but crucially, when the same repertoire of polyclonal Treg was transferred into different recipients, the same clones expanded in each recipient, suggesting that cognate TCR-antigen interactions drive colonic Treg accumulation. Expanded Treg clones were correlated with Treg stability and individual transcriptional states that were maintained in different recipients irrespective of the presence or absence of intestinal inflammation. Our data suggest a role for antigen recognition in the selection and functional specialization of intestinal Treg. We speculate that the therapeutic use of Treg must take into account TCR context-mediated properties to optimise Treg stability and function in vivo.

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Project description:Regulatory T (Treg) cells, whose identity and function are defined by the transcription factor Foxp3, are indispensable for immune homeostasis. It is unclear whether Foxp3 exerts its Treg lineage specification function through active modification of the chromatin landscape and establishment of new enhancers or by exploiting a pre-existing enhancer landscape. Analysis of the chromatin accessibility of Foxp3-bound enhancers in Treg and Foxp3-negative T cells showed that Foxp3 was bound overwhelmingly to pre-accessible enhancers occupied by its cofactors in precursor cells or a structurally related predecessor. Furthermore, the bulk of Foxp3-bound Treg cell enhancers inaccessible in Foxp3- CD4+ cells became accessible upon T cell receptor activation prior to Foxp3 expression with only a small subset associated with several functionally important genes being exclusively Treg cell-specific. Thus, in a late cellular differentiation process Foxp3 defines Treg cell functionality in an “opportunistic” manner by largely exploiting the preformed enhancer network instead of establishing a new enhancer landscape. Array expression. Three cell types with 3-5 replicates each.

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Project description:Regulatory T (Treg) cells, whose identity and function are defined by the transcription factor Foxp3, are indispensable for immune homeostasis. It is unclear whether Foxp3 exerts its Treg lineage specification function through active modification of the chromatin landscape and establishment of new enhancers or by exploiting a pre-existing enhancer landscape. Analysis of the chromatin accessibility of Foxp3-bound enhancers in Treg and Foxp3-negative T cells showed that Foxp3 was bound overwhelmingly to pre-accessible enhancers occupied by its cofactors in precursor cells or a structurally related predecessor. Furthermore, the bulk of Foxp3-bound Treg cell enhancers lacking in Foxp3- CD4+ cells became accessible upon T cell receptor activation prior to Foxp3 expression with only a small subset associated with several functionally important genes being exclusively Treg cell-specific. Thus, in a late cellular differentiation process Foxp3 defines Treg cell functionality in an “opportunistic” manner by largely exploiting the preformed enhancer network instead of establishing a new enhancer landscape. Four transcription factors (Foxp3, Ets1, Elf1, and Cbfb) were immunoprecipated while crosslinked to chromatin. These experiments were then combined with DNase-seq data (being uploaded separately as part of ENCODE project) to find that Foxp3 binds exclusively to open chromatin. Data was also leveraged from GSE40657 and GSE33653.

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A Unique Epigenomic Landscape Defines Human Erythropoiesis (RNA-seq)

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Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification

Project description:This SuperSeries is composed of the following subset Series: GSE40684: Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification [ChIP-Seq] GSE40685: Foxp3 exploits a preexistent enhancer landscape for regulatory T cell lineage specification [Expression] Refer to individual Series

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