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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO Tr1 ATAC-seq]

ABSTRACT: IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO Tr1 ATAC-seq]

PROVIDER: PRJNA666212 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12735605_1.fastq.gz	Fastqsanger.gz
	SRR12735605_2.fastq.gz	Fastqsanger.gz
	SRR12735606_1.fastq.gz	Fastqsanger.gz
	SRR12735606_2.fastq.gz	Fastqsanger.gz
	SRR12735607_1.fastq.gz	Fastqsanger.gz

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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO Tr1 ATAC-seq]

Project description:IL-27 is an immunoregulatory cytokine that suppresses inflammation through multiple mechanisms including induction of IL-10, but the transcriptional network mediating its diverse functions remains unclear. Combining temporal RNA profiling with computational algorithms, we predict 79 transcription factors induced by IL-27 in T cells. We validate 11 known and discover 5 positive (Cebpb, Fosl2, Tbx21, Hlx, Atf3) and 2 negative (Irf9, Irf8) Il10 regulators, generating an experimentally refined regulatory network for Il10. We report two central regulators Prdm1 and Maf that cooperatively drive the expression of signature genes induced by IL-27 in Type 1 regulatory T cells, mediate IL-10 expression in all T helper cells, and determine the regulatory phenotype of colonic Foxp3+regulatory T cells. Prdm1/Maf double-knockout mice develop spontaneous colitis, phenocopying the ll10 deficient mice. Our work provides insights for IL-27 driven transcriptional networks and identifies two shared Il10 regulators that orchestrate immunoregulatory programs across T helper cell subsets.

2020-12-21 | GSE158701 | GEO

IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

2020-12-21 | GSE158967 | GEO

IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Tr1 differentiation with IL-27 microarray]

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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Tr1 deficient in TFs RNA-seq]

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IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets [IL10+ vs IL10-T helper cell RNA-seq]

2020-12-21 | GSE158703 | GEO

IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

Project description:IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Prdm1/Maf KO colonic CD4 T cells scRNA-seq]

| PRJNA667100 | ENA

IL-10 Receptor Signaling is essental for Tr1 cell function in vivo

Project description:Interleukin-10 (IL-10) is essential to maintain intestinal homeostasis. CD4+ T regulatory type 1 (TR1) cells produce large amounts of this cytokine and being therefore currently examined in clinical trials as T-cell therapy in patients with inflammatory bowel disease (IBD). However, factors and molecular signals sustaining TR1 cell regulatory activity still need to be identified in order to optimize the efficiency and to ensure the safety of these trials. We investigated the role of IL-10 signaling in mature TR1 cells in vivo. Double IL-10eGFP Foxp3mRFP reporter mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity of TR1 cells in a murine IBD model, a model that resembles the trials performed in humans. The molecular signaling was elucidated in vitro. Finally, we used human TR1 cells, currently employed for cell therapy, to confirm our results. We found that murine TR1 cells expressed functional IL-10 receptor α. TR1 cells with impaired IL-10 receptor signaling lost their regulatory activity in vivo. TR1 cells required IL-10 receptor signaling in order to activate p38 MAP kinase, thereby sustaining IL-10 production, which ultimately mediated their suppressive activity. Finally, we confirmed these data using human TR1 cells. In conclusion TR1 cell regulatory activity is dependent on IL-10 receptor signaling. These data suggest that in order to optimize TR1 cell-based therapy, IL-10 receptor expression has to be taken into consideration.

2016-12-30 | GSE89080 | GEO

IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Tr1 differentiation with IL-27 microarray]

Project description:IL-27 driven transcriptional network identifies regulators of IL-10 expression across T helper cell subsets[Tr1 differentiation with IL-27 microarray]

| PRJNA667947 | ENA

Prdm1

Project description:Prdm1

| PRJNA300302 | ENA

Comprehensive mapping of epigenetic events during the T-follicular helper-to-T-regulatory type-1 transdifferentiation pathway reveal a global poised state

Project description:Chronic antigenic stimulation can trigger the formation of IL-10-producing T-regulatory type 1 (TR1) cells in vivo. We have recently shown that T follicular helper cells are precursors of TR1 cells and that the TFH-to-TR1 cell transdifferentiation process is underpinned by the progressive loss and acquision of opposing transcription factor gene expression programs that evolve through at least one transitional cell stage. Through a combination of wide-ranging bulk and single-cell transcriptional and epigenetic studies, here we demonstrate that TFH cells are epigenetically poised to differentiate into TR1 cells. Specifically, we find that the TFH-to-TR1 cell transition is accompanied by a significant reduction of the open chromatin regions (OCRs) found in TFH cells. However, the OCRs shared by TR1-like and TFH cells have a remarkably similar distribution of H3K27ac-marked active enhancers. Whereas the DNA regions that overlap these active enhancers are closed and hyper-methylated in conventional T cells, they are hypo-methylated in both TFH and TR1-like cells, even in genes silent in TFH cells, such as Il10. Furthermore, these enhancers are enriched for binding sites for the TFH and TR1-associated transcription factors (TFs) TOX-2, IRF4 and c-Maf. These data suggest that TFH cells are epigenetically poised to become TR1 cells, and that sustained TCR ligation-induced chromatin remodeling coupled to the acquisition of an alternative transcription factor expression profile are sufficient to drive their transdifferentiation into TR1 cells.

2024-11-07 | GSE248152 | GEO

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