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Epigenetic profiling in CD4 and CD8 T cells from Graves’ disease patients reveals changes in genes associated with T cell receptor signaling [gene expression]

ABSTRACT: In Graves’ disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71956 | GEO | 2015/11/06

SECONDARY ACCESSION(S): PRJNA292563

REPOSITORIES: GEO

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Epigenetic profiling in CD4 and CD8 T cells from Gravesâ?? disease patients reveals changes in genes associated with T cell receptor signaling [ChIP-seq]

Project description:In Gravesâ?? disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients. Individuals were recruited from the Estonian Genome Center of the University of Tartu. Genomic DNA was extracted from sorted CD4+ (H3K4me3 ChIP: 15 controls and 14 GD patients; H3K27ac ChIP: 11 controls and 13 GD patients) and CD8+ (H3K4me3 ChIP: 17 controls and 14 GD patients; H3K27ac ChIP: 15 controls and 14 GD patients) T cells. The data collection was performed at the SNP&SEQ Technology Platform in Uppsala University, and data analysis was done at the Institute of Biomedicine and Translational Medicine in the University of Tartu.

2015-11-06 | E-GEOD-71952 | biostudies-arrayexpress

Epigenetic profiling in CD4 and CD8 T cells from Gravesâ disease patients reveals changes in genes associated with T cell receptor signaling [gene expression]

Project description:In Gravesâ disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients. Individuals were recruited from the Estonian Genome Center of the University of Tartu. Total RNA was extracted from sorted CD4+ (10 controls and 15 GD patients) and CD8+ (8 controls and 16 GD patients) T cells. The data collection was performed at the Estonian Genome Center Core Facility, and data analyses was done at the Institute of Biomedicine and Translational Medicine in the University of Tartu.

2015-11-06 | E-GEOD-71956 | biostudies-arrayexpress

Epigenetic profiling in CD4 and CD8 T cells from Gravesâ disease patients reveals changes in genes associated with T cell receptor signaling [methylation]

Project description:In Gravesâ disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients. Individuals were recruited from the Estonian Genome Center of the University of Tartu. Genomic DNA was extracted from sorted CD4+ (31 controls and 36 GD patients) and CD8+ (31 controls and 37 GD patients) T cells. The data collection was performed at the SNP&SEQ Technology Platform in Uppsala University, and data analysis was done at the Institute of Biomedicine and Translational Medicine in the University of Tartu.

2015-11-06 | E-GEOD-71955 | biostudies-arrayexpress

Epigenetic profiling in CD4 and CD8 T cells from Graves’ disease patients reveals changes in genes associated with T cell receptor signaling [methylation]

Project description:In Graves’ disease (GD), a combination of genetic, epigenetic and environmental factors causes an autoimmune response to the thyroid gland, characterized by lymphocytic infiltrations and autoantibodies targeting the thyroid stimulating hormone receptor (TSHR) and other thyroid antigens. To identify the epigenetic changes involved in GD, we performed a genome-wide analysis of DNA methylation and enrichment of H3K4me3 and H3K27ac histone marks in sorted CD4+ and CD8+ T cells. We found 365 and 3322 differentially methylated CpG sites in CD4+ and CD8+ T cells, respectively. Among the hypermethylated CpG sites, we specifically found enrichment of genes involved in T cell signaling (CD247, LCK, ZAP70, CD3D, CD3E, CD3G, CTLA4 and CD8A) and decreased expression of CD3 gene family members. The hypermethylation was accompanied with the active chromatin histone modifications as we found decreased signals of H3K4me3 and H3K27ac marks at several T cell signaling genes in ChIP-seq analysis. In addition, we found hypermethylation of the TSHR gene first intron, where several GD-associated polymorphisms are located. Our results demonstrate an involvement of dysregulated DNA methylation and histone modifications at T cell signaling genes in GD patients.

2015-11-06 | GSE71955 | GEO

Epigenetic profiling in CD4 and CD8 T cells from Graves’ disease patients reveals changes in genes associated with T cell receptor signaling [ChIP-seq]

2015-11-06 | GSE71952 | GEO

Microarray profile of CD19+ B cells from Graves' disease patients reveals potential molecular mechanisms associated with the proliferation of B cell

Project description:Hyperthyroidism is a kind of common autoimmune disease. It is widely accepted that B lymphocytes play a significant role in GD as they are the source of autoantibodies (TRAb) against the thyroid-stimulating hormone receptor (TSHR). We previously observed B cells infiltrated in the thyroid tissue from GD patients was significantly higher than that in healthy controls.In this study, our flow cytometry results indicated that the proportion of B cells in GD patients is much higher than that in control. To explore the underlying pathological function of B cells in GD, a microarray profiles was performed in these isolated B cells.

2019-09-02 | GSE136709 | GEO

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (ChIP-seq)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. ChIP-seq analysis for distribution of H3K4me1, H3K27ac, and H3K4me3 histone marks in in vitro-grown hematopoietic cells transduced with AML1-ETO

2015-04-22 | E-GEOD-59580 | biostudies-arrayexpress

Genome-wide maps of chromatin state in human erythroblasts differentiated from CD34+ cells.

Project description:Treatment with thyroid hormone receptor beta agonist, GC-1, significantly increased the signal intensities of the top 300 NCOA4 chromatin binding sites, which overlapped with binding sites for Pol II as well as with histone marks associated with active transcription, such as H3K27Ac and H3K4Me3, but not with marks such as H3K4Me1 commonly associated with enhancers

2017-09-06 | GSE102584 | GEO

Impact of human MLL/COMPASS and Polycomb complexes on the DNA methylome [MBD-seq]

Project description:The association of DNA CpG methylation (or its absence) with occupancy of histone post translational modifications has hinted at an underlying crosstalk between histone marks and DNA methylation in patterning the human methylome, an idea supported by corresponding alterations to both histone marks and DNA methylation during malignant transformation. This study investigated the framework by which histone marks influence DNA methylation. Using RNAi in a human pluripotent embryonic carcinoma cell line we depleted essential components of the histone modifying complexes that establish the posttranslational modifications H3K4me3, H3K27me3, and H2AK119ub, and we assayed the impact of the subsequent loss of these marks on the DNA methylome. Absence of H2AK119ub resulted predominantly in hypomethylation across the genome. Removal of H3K4me3 or, surprisingly, H3K27me3 caused CpG island hypermethylation at a subset of loci. Intriguingly, many promoters were co-regulated by all three histone marks, becoming hypermethylated with loss of H3K4me3 or H3K27me3 and becoming hypomethylated with depletion of H2AK119ub, and many of these co-regulated loci were among those that are commonly, aberrantly hypermethylated in cancer.

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