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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [ChIP-seq]

ABSTRACT: Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [ChIP-seq]

PROVIDER: PRJNA445705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6898600.fastq.gz	Fastqsanger.gz
	SRR6898610.fastq.gz	Fastqsanger.gz
	SRR6898620.fastq.gz	Fastqsanger.gz
	SRR6898630.fastq.gz	Fastqsanger.gz
	SRR6898640.fastq.gz	Fastqsanger.gz

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [RNA-seq]

Project description:We generated expression profiles of TH1 and TREG cells from T1D and healthy subjects by RNA-Seq. By integrating RNA-Seq dta with other data sets, we predicted and validated serveral T1D risk SNPs.

2019-03-26 | GSE112341 | GEO

Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes

Project description:Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [ChIP-seq]

Project description:Most type 1 diabets (T1D) associated SNPs are located in non-coding regions, making it hard to understand their functional impact. We performed epigenomic profiling of two enhancer marks, H3K4me1 and H3K27ac, using primary TH1 and TREG cells from healthy and T1D subjects. By integrating enhancers predicted using these ChIP-Seq data, T1D associated SNPs and additional supporting data, we found and validated several novel risk SNPs for T1D.

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [RNA-seq]

Project description:Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [RNA-seq]

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes

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

2019-03-26 | GSE112342 | GEO

Risk variants disrupting enhancers of TH1 and TREG cells in type 1 diabetes.

Project description:Genome-wide association studies (GWASs) have revealed 59 genomic loci associated with type 1 diabetes (T1D). Functional interpretation of the SNPs located in the noncoding region of these loci remains challenging. We perform epigenomic profiling of two enhancer marks, H3K4me1 and H3K27ac, using primary TH1 and TREG cells isolated from healthy and T1D subjects. We uncover a large number of deregulated enhancers and altered transcriptional circuitries in both cell types of T1D patients. We identify four SNPs (rs10772119, rs10772120, rs3176792, rs883868) in linkage disequilibrium (LD) with T1D-associated GWAS lead SNPs that alter enhancer activity and expression of immune genes. Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively. Loss of binding by YY1 also results in the loss of long-range enhancer-promoter interaction. These findings provide insights into how noncoding variants affect the transcriptomes of two T-cell subtypes that play critical roles in T1D pathogenesis.

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Blockade of PF4-induced Th1-Treg polarization enhances anti-tumor immunity

Project description:The tumor microenvironment (TME) contains various immune-suppressive cells such as regulatory T cells (Tregs) and M2-like tumor associated macrophages (TAMs) that express the enzyme arginase I (Arg1). T helper 1-polarized Treg (Th1-Treg) is a Treg subset that markedly accumulate in tumor tissues, suppressing anti-tumor immunity. However, little is known about the mechanism behind the abundant presence of Th1-Tregs in TME. Here we show that Arg1-expressing TAMs (Arg1+ TAMs) play critical roles for the high Th1-Treg ratio in TME. Selective depletion of Arg1+ TAMs using the VeDTR system inhibited tumor growth and concurrently reduced the Th1-Treg ratio in TME. Notably, Arg1+ TAMs secreted platelet factor 4 (PF4) that polarized Tregs to Th1-Tregs in a CXCR3-dependent manner. Both genetic PF4 inactivation and PF4 neutralization hindered Th1-Treg accumulation in TME, consequently suppressing tumor growth. Collectively, our study highlights the importance of M2-like TAM-produced PF4 for high Th1-Treg levels in TME to suppress anti-tumor immunity, and demonstrates PF4 neutralization as a potential cancer immunotherapeutic strategy by intervening the M2-like TAM/Th1-Treg axis.

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Project description:CD4+Foxp3+ Treg cells are essential for maintaining self-tolerance and preventing excessive immune responses. In the context of Th1 immune responses, co-expression of the Th1 transcription factor T-bet with Foxp3 is essential for Treg cells to control Th1 responses. T-bet-dependent expression of CXCR3 directs Tregs to the site of inflammation, however, the suppressive mediators enabling effective control of Th1 responses at this site are unknown. In this study, we determined the signature of CXCR3+ Treg cells arising in Th1 settings and defined universal features of Treg cells in this context using multiple Th1-dominated models. Our analysis defined a set of Th1-specific co-inhibitory receptors that are specifically expressed in Treg cells during Th1 immune responses. Among these, we identified the novel co-inhibitory receptor CD85k as a functional mediator of the enhanced suppression of Th1 effector cells by CXCR3+ Treg cells.

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Project description:The immune system comprises various cell types including regulatory T (Treg) cells, and their subsets. Since most of inducible depletion of immune cells for the functional analysis rely on a single protein or gene, it is no longer optimal for the analysis of cell subsets defined by multiple genes. Here we create the Cre- and Flp-double recombinase-dependent intersectional genetic VeDTR mouse system that can selectively label and inducibly deplete a subpopulation of Treg cells called T helper 1 (Th1)-Treg cells. Characterization of Th1-Treg cells using the VeDTR mice revealed the high resistance under oxidative stress, which was required for Th1-Treg cells to accumulate in tumor tissues. Moreover, short-term depletion of Th1-Treg cells only led to anti-tumor immunity but not autoimmunity, whereas that of whole Treg cells did both. Collectively, we have established a novel intersectional genetic immune cell depletion system to reveal unique features of Th1-Treg cells in tumor immunity.

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Blockade of PF4-induced Th1-Treg polarization enhances anti-tumor immunity (Bulk RNA-Seq)

Project description:The tumor microenvironment (TME) contains various immune-suppressive cells such as T helper 1-polarized regulatory T cells (Th1-Tregs). However, little is known about the mechanism behind the abundant presence of Th1-Tregs in TME. In this work, we demonstrate that selective depletion of arginase I (Arg1)-expressing tumor associated macrophages (Arg1+ TAMs) inhibits tumor growth and concurrently reduces the Th1-Treg ratio in TME. Notably, Arg1+ TAMs secrete platelet factor 4 (PF4) that reinforces interferon-γ (IFN-γ)-induced Treg polarization into Th1-Tregs in a manner dependent on CXCR3 and the IFN-γ receptor. Both genetic PF4 inactivation and PF4 neutralization hinder Th1-Treg accumulation in TME, consequently suppressing tumor growth. Collectively, our study highlights the importance of Arg1+ TAM-produced PF4 for high Th1-Treg levels in TME to suppress anti-tumor immunity, and demonstrates PF4 neutralization as a potential cancer immunotherapeutic strategy.

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