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Ro60 iCLIP

ABSTRACT: Autoantibodies target the RNA-binding protein Ro60 in systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, whether Ro60 and its associated RNAs contribute to disease pathogenesis is unclear. We catalogued the Ro60-associated RNAs in human cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72500 | GEO | 2015/09/16

SECONDARY ACCESSION(S): PRJNA294175

REPOSITORIES: GEO

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Ro60 iCLIP

Project description:Autoantibodies target the RNA-binding protein Ro60 in systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, whether Ro60 and its associated RNAs contribute to disease pathogenesis is unclear. We catalogued the Ro60-associated RNAs in human cell lines. iCLIP in 2 cell lines (GM12878, K562).

2015-09-16 | E-GEOD-72500 | biostudies-arrayexpress

RNA-seq of peripheral blood mononuclear cell (PBMC) derived from normal healthy donors and systemic lupus erythematosus (SLE) patients

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

RNA-seq study reveals unique transcriptome expression in systemic lupus erythematosus patients with distinct autoantibody profile

Project description:Systemic lupus erythematosus patients exhibit remarkable heterogeneity in clinical manifestations and autoantibody repertoires. This complexity poses major barrier in diagnosis and effective treatment of SLE. To address this we studied the SLE patients in groups categorized on the basis of distinct sera autoantibodies. SLE patients were segregated into three group based on the presence of autoantibodies against i) dsDNA only ii) ENA (extractable nuclear antigens) only or iii) both.

2016-11-17 | GSE80183 | GEO

Hypomethylation of STAT1 and HLA-DRB1 is associated with type-I interferon-dependent HLA-DRB1 expression in lupus CD8+ T cells

Project description:Systemic lupus erythematosus (SLE) is a chronic relapsing autoimmune disease characterized by the production of autoantibodies and multiple organ involvement. In this study, we investigated genome-wide DNA methylation changes in the CD8+ T cells from 8 pairs of lupus patients compared to age, sex, and ethnicity matched healthy controls.

2019-11-26 | GSE123003 | GEO

Activation of the Interferon Pathway is Dependent upon Autoantibodies in African-American SLE Patients, but not in European-American SLE Patients

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

2013-11-15 | GSE50635 | GEO

Single cell Ig VDJ sequencing (10X Genomics) of human blood B cells from SLE pateints and healthy controls

Project description:B cells positive for Ig kappa and Ig lambda are observed by flow cytometry in one fourth of patients with Systemic Lupus Erythematosus (SLE). Single cell Ig VDJ sequencing (10X Genomics) reveals that kappa/lambda B cells are at the same frequency (about 1.5%) in these SLE patients as in healthy controls. Cells observed by flow cytometry are instead decorated with VH4-34 IgM (kappa or lambda) autoantibodies that are present in some but not all SLE patients.

2022-01-26 | GSE183051 | GEO

Oxidized mitochondrial nucleoids released by neutrophils drive type I Interferon production in human lupus

Project description:Autoantibodies against nucleic acids and excessive type I Interferon (IFN) are hallmarks of human Systemic Lupus Erythematosus (SLE). We previously reported that SLE neutrophils, exposed to TLR7-agonist autoantibodies, release interferogenic DNA, which we now demonstrate to be of mitochondrial origin. We further show that healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage. Rather, they extrude mitochondrial components, including DNA (mtDNA), devoid of oxidized residues. When MtDNA undergoes oxidation, it is directly routed to lysosomes for degradation. This rerouting requires dissociation from the transcription factor TFAM, a dual high mobility group (HMG) protein involved in maintenance and compaction of the mitochondrial genome into nucleoids. Exposure of SLE neutrophils, or healthy IFNprimed neutrophils, to anti-RNP autoantibodies blocks TFAM phosphorylation, a necessary step for nucleoid dissociation. Consequently, oxidized nucleoids accumulate within mitochondria and are eventually extruded as potent interferogenic complexes. In support of the in vivo relevance of this phenomenon, mitochondrial retention of oxidized nucleoids is a feature of SLE blood neutrophils, and autoantibodies against oxidized mtDNA are present in a fraction of patients. This pathway represents a novel therapeutic target in human SLE. 4 samples, no replicates, 2 controls. 2 samples are Neutrophils cultured with and without CCCP (control). 2 samples are Monocytes cultured with and without CCCP (control).

2016-04-07 | E-GEOD-78243 | biostudies-arrayexpress

Gene expression profilings of naive B cell, memory B cell and plasmablast of healthy donors and SLE patients

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

DNA methylation in SLE-related autoantibodies

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

Restoration of regulatory and effector T cell balance and B cell homeostasis in systemic lupus erythematosus patients through vitamin D supplementation

Project description:Systemic lupus erythematosus (SLE) is a T and B cell-dependent autoimmune disease characterized by the appearance of autoantibodies, a global regulatory T cells (Tregs) depletion and an increase in Th17 cells. Recent studies have shown the multifaceted immunomodulatory effects of vitamin D, notably the expansion of Tregs and the decrease of Th1 and Th17 cells. A significant correlation between higher disease activity and lower serum 25-hydroxyvitamin D levels was also shown. This preliminary study suggests the beneficial role of vitamin D in SLE patients and needs to be confirmed in randomized controlled trials. In this prospective study, we evaluated the safety and the immunological effects of vitamin D supplementation in 20 SLE patients with hypovitaminosis D using transcriptomic study at M0 and M2.

2012-03-29 | E-GEOD-36941 | biostudies-arrayexpress

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