DNA methylation profiles profiles of B cell subsets from healthy and SLE subjects
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE118255 | GEO | 2019/05/17
REPOSITORIES: GEO
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Project description:SLE is characterized by the production of autoantibodies that arise from the B cell lineage. Therefore, we sought to assess the epigenetic and transcriptome profiles of distinct B cell subsets known to be expanded in SLE from healthy and SLE subjects. These data define the differentiation heirarchy of B cell subsets and the epigenetic and transcriptional consequences of SLE on human B cells.
2019-05-17 | GSE118254 | GEO
Project description:SLE is characterized by the production of autoantibodies that arise from the B cell lineage. Therefore, we sought to assess the epigenetic and transcriptome profiles of distinct B cell subsets known to be expanded in SLE from healthy and SLE subjects. These data define the differentiation heirarchy of B cell subsets and the epigenetic and transcriptional consequences of SLE on human B cells.
2019-05-17 | GSE118253 | GEO
Project description:Transcriptome profiles of B cell subsets from healthy and SLE subjects
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Project description:DNA methylation profiles profiles of B cell subsets from healthy and SLE subjects
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Project description:Accessible chromatin profiles of B cell subsets from healthy and SLE subjects
| PRJNA484964 | ENA
Project description:<p>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can have debilitating effects on multiple organ systems. In SLE, the pivotal immunologic disturbance is the formation of autoantibodies directed against nuclear and cellular antigens. These autoantibodies are associated with specific organ manifestations. Our previous work has shown that certain single nucleotide polymorphisms (SNPs) are associated with the production of SLE-related autoantibodies. However, these genetic associations do not completely explain autoantibody development in SLE. Therefore, we examined whether epigenetic factors such as DNA methylation may be associated with the development of SLE-related autoantibodies.</p> <p>In this study, we examined whether differential DNA methylation is associated with anti-dsDNA, anti-SSA/Ro, anti-Smith, and anti-RNP autoantibodies. Using the Illumina HumanMethylation450 Beadchip, over 450,000 DNA methylation sites were characterized in 325 female SLE cases of European descent. Using a multivariable regression analyses, the methylation status of 16 CpG sites in 11 genes was found to be associated with the SLE-related autoantibodies under study. This study shows that epigenetic factors are associated with autoimmune disease phenotypes, and epigenetic studies are a complementary method to genetic association studies for understanding the biologic mechanisms contributing to autoimmune disease.</p>
| phs000947 | dbGaP
Project description:Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by production of various pathogenic autoantibodies. Increased type I interferon signature is suggested as a trigger of the disease. Previous studies identify increased plasmablasts in peripheral blood of SLE patients. In spite of the unique cellular properties of the plasmablasts compared with other B cell subsets and plasma cells, the biological characteristics of SLE plasmblast remain unknown and few therapeutic strategies targeting SLE plasmablasts have been applicated. We performed microarray analysis of naive, memory B cells and plasmablasts (CD38+CD43+ B cells) freshly isolated from healthy controls and active SLE (n=4, each) to find the unique biological properties of SLE plasmablast.
2020-08-25 | GSE156751 | GEO
Project description:Background/Purpose: Systemic lupus erythematosus (SLE) is a complex multi-system autoimmune disease of uncertain etiology. Patients from different ancestral backgrounds demonstrate differences in clinical manifestations and autoantibody profiles. In this study we examined genome-wide transcriptional patterns in major immune cell subsets across different ancestral backgrounds. Methods: Peripheral blood was collected from 21 African-American (AA) and 21 European-American (EA) SLE patients, 5 AA controls, and 5 EA controls. CD4+ T-cells, CD8+ T-cells, monocytes and B cells were purified by flow sorting. Each cell subset from each subject was run on an Illumina HumanHT-12 V4 expression BeadChip array (n=208 arrays). Differentially expressed genes (DEGs) were determined by comparing cases and controls of the same ancestral background. Results: The overlap in DEG lists between different cell types from the same ancestral background was very modest (<1%). Typically between 5-10% of DEGs were shared when comparing the same cell type between different ancestral backgrounds (for ex. CD20 AA vs. CD20 EA). Quantitative measurement of global IFN-stimulated gene (ISG) expression revealed that AA subjects demonstrated more concordance across all studied cell types. Two subgroups of patients were identified based on the ISG expression profiles. One subgroup showed higher ISGs expression in all cell types, and the other subgroup had higherISG expression only in T and B lymphocytes but not in monocytes. The correlation of ISG expression with medication data revealed that only the B cells had lower ISG expression in patients taking immunosuppressants, while ISG expression in the other cell types did not differ based upon medication use. Conclusion: We find striking differences in gene expression between different immune cell subsets and between ancestral backgrounds in SLE patients. The IFN signature is diverse, with different transcripts represented in different cell populations, and signature-positive cell subsets differed in EA vs. AA patients. We also find that treatment with the immunosuppressive agents correlates with the down-regulation of B cell ISG expression, and this was not observed in other cell types. Peripheral blood was collected from 21 African-American (AA) and 21 European-American (EA) SLE patients, 5 AA controls, and 5 EA controls. CD4+ T-cells, CD8+ T-cells, monocytes and B cells were purified by flow sorting. Each cell subset from each subject was run on an Illumina HumanHT-12 V4 expression BeadChip array (n=208 arrays).
2015-05-15 | E-GEOD-55447 | biostudies-arrayexpress
Project description:Background/Purpose: Systemic lupus erythematosus (SLE) is a complex multi-system autoimmune disease of uncertain etiology. Patients from different ancestral backgrounds demonstrate differences in clinical manifestations and autoantibody profiles. In this study we examined genome-wide transcriptional patterns in major immune cell subsets across different ancestral backgrounds. Methods: Peripheral blood was collected from 21 African-American (AA) and 21 European-American (EA) SLE patients, 5 AA controls, and 5 EA controls. CD4+ T-cells, CD8+ T-cells, monocytes and B cells were purified by flow sorting. Each cell subset from each subject was run on an Illumina HumanHT-12 V4 expression BeadChip array (n=208 arrays). Differentially expressed genes (DEGs) were determined by comparing cases and controls of the same ancestral background. Results: The overlap in DEG lists between different cell types from the same ancestral background was very modest (<1%). Typically between 5-10% of DEGs were shared when comparing the same cell type between different ancestral backgrounds (for ex. CD20 AA vs. CD20 EA). Quantitative measurement of global IFN-stimulated gene (ISG) expression revealed that AA subjects demonstrated more concordance across all studied cell types. Two subgroups of patients were identified based on the ISG expression profiles. One subgroup showed higher ISGs expression in all cell types, and the other subgroup had higherISG expression only in T and B lymphocytes but not in monocytes. The correlation of ISG expression with medication data revealed that only the B cells had lower ISG expression in patients taking immunosuppressants, while ISG expression in the other cell types did not differ based upon medication use. Conclusion: We find striking differences in gene expression between different immune cell subsets and between ancestral backgrounds in SLE patients. The IFN signature is diverse, with different transcripts represented in different cell populations, and signature-positive cell subsets differed in EA vs. AA patients. We also find that treatment with the immunosuppressive agents correlates with the down-regulation of B cell ISG expression, and this was not observed in other cell types.
2015-05-15 | GSE55447 | GEO
Project description:Systemic lupus erythematosus (SLE), also known simply as lupus, is an autoimmune disease. There is no cure for SLE. The mechanism involves an immune response by autoantibodies against a person's own tissues. However, the mechanism underlying imbalance of autoantibodies is not clear. In this experiment, peripheral blood was obtained from normal healthy donors and systemic lupus erythematosus (SLE) patients. Peripheral blood mononuclear cells (PBMC) were separated by Ficoll separation solution. Samples of four (total eight) donors were pooled and Samples of four (total eight) SLE patients were pooled. The aim was to characterize the mRNA profile of SLE patients compared to healthy donors and find the new target of diagnosis or treatment for SLE.
2020-08-14 | E-MTAB-7145 | biostudies-arrayexpress