Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling
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 iden...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Limbach, Maia [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
11 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Influence of the wind farm integration on load flow and voltage in electrical power system - imen, Labed ELSEVIER, 2016, London |
|---|---|
| Übergeordnetes Werk: |
volume:67 ; year:2016 ; pages:46-56 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.jaut.2015.09.006 |
|---|
| Katalog-ID: |
ELV024529826 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV024529826 | ||
| 003 | DE-627 | ||
| 005 | 20230625143027.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2016 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.jaut.2015.09.006 |2 doi | |
| 028 | 5 | 2 | |a GBVA2016013000003.pica |
| 035 | |a (DE-627)ELV024529826 | ||
| 035 | |a (ELSEVIER)S0896-8411(15)30045-7 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 660 |q VZ |
| 082 | 0 | 4 | |a 620 |q VZ |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.94 |2 bkl | ||
| 100 | 1 | |a Limbach, Maia |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| 264 | 1 | |c 2016transfer abstract | |
| 300 | |a 11 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a 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 decreased levels 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. | ||
| 520 | |a 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 decreased levels 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. | ||
| 650 | 7 | |a Graves' disease |2 Elsevier | |
| 650 | 7 | |a DNA methylation |2 Elsevier | |
| 650 | 7 | |a Epigenetics |2 Elsevier | |
| 650 | 7 | |a T cell signaling |2 Elsevier | |
| 650 | 7 | |a TSHR |2 Elsevier | |
| 700 | 1 | |a Saare, Mario |4 oth | |
| 700 | 1 | |a Tserel, Liina |4 oth | |
| 700 | 1 | |a Kisand, Kai |4 oth | |
| 700 | 1 | |a Eglit, Triin |4 oth | |
| 700 | 1 | |a Sauer, Sascha |4 oth | |
| 700 | 1 | |a Axelsson, Tomas |4 oth | |
| 700 | 1 | |a Syvänen, Ann-Christine |4 oth | |
| 700 | 1 | |a Metspalu, Andres |4 oth | |
| 700 | 1 | |a Milani, Lili |4 oth | |
| 700 | 1 | |a Peterson, Pärt |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |a imen, Labed ELSEVIER |t Influence of the wind farm integration on load flow and voltage in electrical power system |d 2016 |g London |w (DE-627)ELV014127067 |
| 773 | 1 | 8 | |g volume:67 |g year:2016 |g pages:46-56 |g extent:11 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.jaut.2015.09.006 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.94 |j Hals-Nasen-Ohrenheilkunde |q VZ |
| 951 | |a AR | ||
| 952 | |d 67 |j 2016 |h 46-56 |g 11 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
m l ml |
|---|---|
| matchkey_str |
limbachmaiasaaremariotserelliinakisandka:2016----:pgntcrflnic4nc8clsrmrvsiesptetrvashneignsso |
| hierarchy_sort_str |
2016transfer abstract |
| bklnumber |
44.94 |
| publishDate |
2016 |
| allfields |
10.1016/j.jaut.2015.09.006 doi GBVA2016013000003.pica (DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Limbach, Maia verfasserin aut Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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 decreased levels 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. 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 decreased levels 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. Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier Saare, Mario oth Tserel, Liina oth Kisand, Kai oth Eglit, Triin oth Sauer, Sascha oth Axelsson, Tomas oth Syvänen, Ann-Christine oth Metspalu, Andres oth Milani, Lili oth Peterson, Pärt oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:67 year:2016 pages:46-56 extent:11 https://doi.org/10.1016/j.jaut.2015.09.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 67 2016 46-56 11 045F 610 |
| spelling |
10.1016/j.jaut.2015.09.006 doi GBVA2016013000003.pica (DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Limbach, Maia verfasserin aut Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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 decreased levels 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. 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 decreased levels 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. Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier Saare, Mario oth Tserel, Liina oth Kisand, Kai oth Eglit, Triin oth Sauer, Sascha oth Axelsson, Tomas oth Syvänen, Ann-Christine oth Metspalu, Andres oth Milani, Lili oth Peterson, Pärt oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:67 year:2016 pages:46-56 extent:11 https://doi.org/10.1016/j.jaut.2015.09.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 67 2016 46-56 11 045F 610 |
| allfields_unstemmed |
10.1016/j.jaut.2015.09.006 doi GBVA2016013000003.pica (DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Limbach, Maia verfasserin aut Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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 decreased levels 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. 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 decreased levels 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. Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier Saare, Mario oth Tserel, Liina oth Kisand, Kai oth Eglit, Triin oth Sauer, Sascha oth Axelsson, Tomas oth Syvänen, Ann-Christine oth Metspalu, Andres oth Milani, Lili oth Peterson, Pärt oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:67 year:2016 pages:46-56 extent:11 https://doi.org/10.1016/j.jaut.2015.09.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 67 2016 46-56 11 045F 610 |
| allfieldsGer |
10.1016/j.jaut.2015.09.006 doi GBVA2016013000003.pica (DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Limbach, Maia verfasserin aut Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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 decreased levels 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. 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 decreased levels 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. Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier Saare, Mario oth Tserel, Liina oth Kisand, Kai oth Eglit, Triin oth Sauer, Sascha oth Axelsson, Tomas oth Syvänen, Ann-Christine oth Metspalu, Andres oth Milani, Lili oth Peterson, Pärt oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:67 year:2016 pages:46-56 extent:11 https://doi.org/10.1016/j.jaut.2015.09.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 67 2016 46-56 11 045F 610 |
| allfieldsSound |
10.1016/j.jaut.2015.09.006 doi GBVA2016013000003.pica (DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Limbach, Maia verfasserin aut Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier 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 decreased levels 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. 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 decreased levels 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. Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier Saare, Mario oth Tserel, Liina oth Kisand, Kai oth Eglit, Triin oth Sauer, Sascha oth Axelsson, Tomas oth Syvänen, Ann-Christine oth Metspalu, Andres oth Milani, Lili oth Peterson, Pärt oth Enthalten in Academic Press imen, Labed ELSEVIER Influence of the wind farm integration on load flow and voltage in electrical power system 2016 London (DE-627)ELV014127067 volume:67 year:2016 pages:46-56 extent:11 https://doi.org/10.1016/j.jaut.2015.09.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.94 Hals-Nasen-Ohrenheilkunde VZ AR 67 2016 46-56 11 045F 610 |
| language |
English |
| source |
Enthalten in Influence of the wind farm integration on load flow and voltage in electrical power system London volume:67 year:2016 pages:46-56 extent:11 |
| sourceStr |
Enthalten in Influence of the wind farm integration on load flow and voltage in electrical power system London volume:67 year:2016 pages:46-56 extent:11 |
| format_phy_str_mv |
Article |
| bklname |
Hals-Nasen-Ohrenheilkunde |
| institution |
findex.gbv.de |
| topic_facet |
Graves' disease DNA methylation Epigenetics T cell signaling TSHR |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Influence of the wind farm integration on load flow and voltage in electrical power system |
| authorswithroles_txt_mv |
Limbach, Maia @@aut@@ Saare, Mario @@oth@@ Tserel, Liina @@oth@@ Kisand, Kai @@oth@@ Eglit, Triin @@oth@@ Sauer, Sascha @@oth@@ Axelsson, Tomas @@oth@@ Syvänen, Ann-Christine @@oth@@ Metspalu, Andres @@oth@@ Milani, Lili @@oth@@ Peterson, Pärt @@oth@@ |
| publishDateDaySort_date |
2016-01-01T00:00:00Z |
| hierarchy_top_id |
ELV014127067 |
| dewey-sort |
3610 |
| id |
ELV024529826 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV024529826</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625143027.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.jaut.2015.09.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016013000003.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV024529826</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0896-8411(15)30045-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">660</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.94</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Limbach, Maia</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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 decreased levels 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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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 decreased levels 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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Graves' disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DNA methylation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Epigenetics</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">T cell signaling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TSHR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saare, Mario</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tserel, Liina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kisand, Kai</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eglit, Triin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sauer, Sascha</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Axelsson, Tomas</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Syvänen, Ann-Christine</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Metspalu, Andres</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Milani, Lili</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Peterson, Pärt</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="a">imen, Labed ELSEVIER</subfield><subfield code="t">Influence of the wind farm integration on load flow and voltage in electrical power system</subfield><subfield code="d">2016</subfield><subfield code="g">London</subfield><subfield code="w">(DE-627)ELV014127067</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:67</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:46-56</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.jaut.2015.09.006</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.94</subfield><subfield code="j">Hals-Nasen-Ohrenheilkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">67</subfield><subfield code="j">2016</subfield><subfield code="h">46-56</subfield><subfield code="g">11</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Limbach, Maia |
| spellingShingle |
Limbach, Maia ddc 610 ddc 660 ddc 620 bkl 44.94 Elsevier Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| authorStr |
Limbach, Maia |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV014127067 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 660 - Chemical engineering 620 - Engineering & allied operations |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR Elsevier |
| topic |
ddc 610 ddc 660 ddc 620 bkl 44.94 Elsevier Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR |
| topic_unstemmed |
ddc 610 ddc 660 ddc 620 bkl 44.94 Elsevier Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR |
| topic_browse |
ddc 610 ddc 660 ddc 620 bkl 44.94 Elsevier Graves' disease Elsevier DNA methylation Elsevier Epigenetics Elsevier T cell signaling Elsevier TSHR |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
m s ms l t lt k k kk t e te s s ss t a ta a c s acs a m am l m lm p p pp |
| hierarchy_parent_title |
Influence of the wind farm integration on load flow and voltage in electrical power system |
| hierarchy_parent_id |
ELV014127067 |
| dewey-tens |
610 - Medicine & health 660 - Chemical engineering 620 - Engineering |
| hierarchy_top_title |
Influence of the wind farm integration on load flow and voltage in electrical power system |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV014127067 |
| title |
Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| ctrlnum |
(DE-627)ELV024529826 (ELSEVIER)S0896-8411(15)30045-7 |
| title_full |
Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| author_sort |
Limbach, Maia |
| journal |
Influence of the wind farm integration on load flow and voltage in electrical power system |
| journalStr |
Influence of the wind farm integration on load flow and voltage in electrical power system |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2016 |
| contenttype_str_mv |
zzz |
| container_start_page |
46 |
| author_browse |
Limbach, Maia |
| container_volume |
67 |
| physical |
11 |
| class |
610 610 DE-600 660 VZ 620 VZ 610 VZ 44.94 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Limbach, Maia |
| doi_str_mv |
10.1016/j.jaut.2015.09.006 |
| dewey-full |
610 660 620 |
| title_sort |
epigenetic profiling in cd4+ and cd8+ t cells from graves' disease patients reveals changes in genes associated with t cell receptor signaling |
| title_auth |
Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| 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 decreased levels 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. |
| abstractGer |
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 decreased levels 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. |
| abstract_unstemmed |
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 decreased levels 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. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |
| url |
https://doi.org/10.1016/j.jaut.2015.09.006 |
| remote_bool |
true |
| author2 |
Saare, Mario Tserel, Liina Kisand, Kai Eglit, Triin Sauer, Sascha Axelsson, Tomas Syvänen, Ann-Christine Metspalu, Andres Milani, Lili Peterson, Pärt |
| author2Str |
Saare, Mario Tserel, Liina Kisand, Kai Eglit, Triin Sauer, Sascha Axelsson, Tomas Syvänen, Ann-Christine Metspalu, Andres Milani, Lili Peterson, Pärt |
| ppnlink |
ELV014127067 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth oth oth oth |
| doi_str |
10.1016/j.jaut.2015.09.006 |
| up_date |
2024-07-06T21:40:46.827Z |
| _version_ |
1803867439054716928 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV024529826</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625143027.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.jaut.2015.09.006</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016013000003.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV024529826</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0896-8411(15)30045-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">660</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.94</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Limbach, Maia</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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 decreased levels 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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">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 decreased levels 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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Graves' disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DNA methylation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Epigenetics</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">T cell signaling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">TSHR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Saare, Mario</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tserel, Liina</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kisand, Kai</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eglit, Triin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sauer, Sascha</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Axelsson, Tomas</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Syvänen, Ann-Christine</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Metspalu, Andres</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Milani, Lili</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Peterson, Pärt</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="a">imen, Labed ELSEVIER</subfield><subfield code="t">Influence of the wind farm integration on load flow and voltage in electrical power system</subfield><subfield code="d">2016</subfield><subfield code="g">London</subfield><subfield code="w">(DE-627)ELV014127067</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:67</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:46-56</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.jaut.2015.09.006</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.94</subfield><subfield code="j">Hals-Nasen-Ohrenheilkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">67</subfield><subfield code="j">2016</subfield><subfield code="h">46-56</subfield><subfield code="g">11</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.3995075 |