Homo sapiens
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PROVIDER: PRJNA239638 | ENA |
REPOSITORIES: ENA
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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) is a heterogeneous disease which leads to different levels of serum autoantibodies to RNA-binding proteins (anti-RBP) and interferon-α (IFN-α), which plays an important pathogenic role in SLE, between European-American (EA) and African-American (AA) patients. We aimed to explore how IFN-related gene expression pathways differ in patients according to their ancestry and anti-RBP profile Whole blood from 33 female SLE patients and 16 matched controls from EA and AA ancestral backgrounds was analyzed through Affymetrix Gene 1.0 ST gene expression arrays and the data were further studied through Ingenuity Pathways Analysis for canonical pathway comparison. An independent replication cohort of more than 100 SLE patient samples and 30 controls was used to test the hypotheses generated by the microarray data, using qPCR to quantify gene expression.
2013-11-15 | E-GEOD-50635 | biostudies-arrayexpress
Project description:Comparison of two B cell subsets isolated from healthy individuals after stimulation in vitro with SLE-related immune complexes and in the presence of plasmacytoid dendritic cells.
2017-09-07 | E-MTAB-5740 | biostudies-arrayexpress
Project description:To examine mononuclear cell gene expression profiles in patients with and without SLE and subsets with and without atherosclerosis
2012-04-17 | GSE37356 | GEO
Project description:Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by pathogenic auto-antibodies that cause end organ damage. B cells are thought to play a central role in the immunopathogenesis of SLE and display several abnormalities in patients, including a strong type I interferon signature as well as lower expression of surface markers including TLR9 and FcγRIIB. To characterize differences in the proportion of distinct B cell subsets as well as intrinsic transcriptomic differences between B cells from healthy donors and SLE patients, we performed single-cell RNA sequencing on B cells isolated from PBMCs of donors. Several notable features were observed, including a strong interferon response signature among SLE B cells, and the expansion of CD11c+T-bet+ B cell subsets in these patients. Additionally, several surface molecules including MHC Class II proteins and surface proteins such as CD74 and CD52 were found to be differentially expressed in B cells isolated from SLE patients. The differences in B cell subset proportion as well as expression of various genes might play a role in B cell mediated pathogenesis of SLE.
2020-12-14 | GSE163121 | GEO
Project description:To examine mononuclear cell gene expression profiles in patients with and without SLE and subsets with and without atherosclerosis Monocytes were obtained from 20 patients with SLE and 16 healthy controls and were in vitro differentiated into macrophages. Subjects also underwent laboratory and imaging studies of the coronary arteries, carotid arteries, and aorta to evaluate for subclinical atherosclerosis.
2012-04-16 | E-GEOD-37356 | biostudies-arrayexpress
Project description:Systemic lupus erythematosus (SLE) is a complex autoimmune disease with heterogeneous clinical manifestations and the pathogenesis of SLE is still unclear. Various omics results have been reported for SLE, but the molecular hallmarks of SLE, especially in patients with different disease activity, using an integrated multi-omics approach have not been fully investigated. Here, we collected blood samples from 10 healthy controls (HCs) and 40 SLE patients with different clinical activity including inactive (IA), low activity (LA), and high activity (HA). Using an integrative analysis of proteomic, metabolomic and lipidomic profiles, we report the multi-omics landscape for SLE. The molecular changes suggest that both the complement system and the inflammatory response were activated in SLEs and were associated with disease activity. Additionally, activation of the immunoglobulin mediated immune response were observed in the LA stage of the disease, however this immune response was suppressed slightly in the HA stage. Finally, an imbalance in lipid metabolism, especially in sphingolipid metabolism, accompanied with dysregulated apolipoproteins were observed to contribute to the disease activity of SLE. The multi-omics data presented in this study and the characterization of peripheral blood from SLE patients may thus help provide important clues regarding the pathogenesis of SLE.
2022-03-02 | PXD031979 | iProX
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:We previously reported the establishment of a rabbit (Oryctolagus cuniculus) model of Systemic Lupus Erythematosus (SLE) in which peptide immunization led to lupus-like autoantibody production including anti-Sm, -RNP, -SS-A, -SS-B and -dsDNA. Some neurological symptoms in form of seizures and nystagmus were observed. The animals used in the previous and in the present study were from a National Institute of Allergy and Infectious Diseases colony of rabbits that were pedigreed, immunoglobulin allotype-defined but not inbred. Their genetic heterogeneity may correspond to that found among patients of a given ethnicity. We extended the information about this rabbit model of SLE by microarray based expression profiling. We first demonstrated that human expression arrays could be used with rabbit RNA to yield information on molecular pathways. We then designed a study evaluating gene expression profiles in 8 groups of control and SLE rabbits (46 rabbits in total). Genes significantly upregulated in SLE rabbits were associated with NK cytotoxicity, antigen presentation, leukocyte migration, cytokine activity, protein kinases, RNA spliceosomal ribonucleoproteins, intracellular signaling cascades, and glutamate receptor activity. These results link increased immune activation with up-regulation of components associated with neurological and anti-RNP responses, demonstrating the utility of the rabbit SLE model to uncover biological pathways related to SLE-induced clinical symptoms, including Neuropsychiatric Lupus. Our finding of distinct gene expression patterns in rabbits that made anti-dsDNA compared to those that only made other anti-nuclear antibodies should be further investigated in subsets of SLE patients with different autoantibody profiles.
2010-07-23 | GSE23076 | GEO