Single cell 'omics resolves transcriptional alterations in Sjogren's Syndrome
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PROVIDER: PRJNA733527 | ENA |
REPOSITORIES: ENA
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Project description:Single cell 'omics resolves transcriptional alterations in Sjogren's Syndrome
| PRJNA733528 | ENA
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease.
2017-05-01 | GSE77599 | GEO
Project description:A study was designed to further define the viral landscape within Sjogren's Syndrome (pSS) affected salivary gland tissue to identify potential viral-mediated triggers in the pathogenesis of this autoimmune disease. Viral Probes for Vertebrate Infecting Viral Families
2017-05-01 | E-GEOD-77599 | biostudies-arrayexpress
Project description:We performed autoantigen arrays on sera derived from Sjogren's syndrome mice that lacked Myd88 systemically (NOD.B10LSL-/- strain) or lacked Myd88 in specific tissues (NOD.B10Myd88delta and NOD.B10LSL-/-Vav+ strains). We also examined sera from Myd88-sufficient controls (NOD.B10Myd88fl/fl, NOD.B10, and NOD.B10LSL+/- strains).
2021-01-25 | GSE163395 | GEO
Project description:Multi-omics study was conducted to elucidate the crucial molecular mechanisms of primary Sjögren’s syndrome (SS) pathology. We generated multiple data set from well-defined patients with SS, which includes whole-blood transcriptomes, serum proteomes and peripheral immunophenotyping. Based on our newly generated data, we performed an extensive bioinformatic investigation. Our integrative analysis identified SS gene signatures (SGS) dysregulated in widespread omics layers, including epigenomes, mRNAs and proteins. SGS predominantly involved the interferon signature and ADAMs substrates. Besides, SGS was significantly overlapped with SS-causing genes indicated by a genome-wide association study and expression trait loci analyses. Combining the molecular signatures with immunophenotypic profiles revealed that cytotoxic CD8 T cells were associated with SGS. Further, we observed the activation of SGS in cytotoxic CD8 T cells isolated from patients with SS. Our multi-omics investigation identified gene signatures deeply associated with SS pathology and showed the involvement of cytotoxic CD8 T cells. These integrative relations across multiple layers will facilitate our understanding of SS at the system level. Proteomics and FACS data will be found in Synapse. https://www.synapse.org/#!Synapse:syn8483276
2017-05-19 | GSE84844 | GEO
Project description:Sera were acquired from the Sjogren's International Collaborative Clinical Alliance (SICCA) biorepository and were assayed for IgG autoantibodies. The autoantigen array was performed to identify the specific autoantibodies that were enriched in pSS patients.
2023-10-24 | GSE236254 | GEO
Project description:Autoantibodies in sera from Sjogren's syndrome mice
| PRJNA685989 | ENA
Project description:To study the gene expression profile of salivary glands with varying degrees of inflammation in Sjogren's and non Sjogren's patients
2011-05-01 | GSE23117 | GEO
Project description:Spleens (n = 2-3) were harvested from mice with primary Sjogren's syndrome (NOD.B10) and cells were sort-purified. Follicular B cells (FO) (6 million), Marginal zone B cells (4.5 million) and age-associated B cells (500,000) were sorted. Cells were cultured in 200 uL of complete RPMI media containing 62.5 ng/mL of imiquimod, a TLR7 agonist. Cells were cultured for 6 days, and the supernatants were harvested and stored at -20 C. Samples were shipped to UT Southwestern for autoantigen array analysis.
2023-10-24 | GSE236255 | GEO
Project description:The objective of the study was to identify gene expression signatures in minor salivary glands (MSGs) from patients with primary Sjogren's syndrome (SS). METHODS: A 16K complementary DNA microarray was used to generate gene expression profiles in MSGs obtained from 10 patients with primary SS and 10 control subjects. The data were analyzed by 2 different strategies, one strict primary analysis and one subanalysis that allowed for inclusion of genes with no signal in more than 3 samples from each group. The results were validated by quantitative reverse transcriptase-polymerase chain reaction techniques. RESULTS: We found a distinct difference in gene expression levels in MSGs, enabling a simple class prediction method to correctly classify 19 of the 20 samples as either patient or control, based on the top 5 differentially expressed genes. The 50 most differentially expressed genes in the primary SS group compared with the control group were all up-regulated, and a clear pattern of genes involved in chronic inflammation was found. CXCL13 and CD3D were expressed in >/=90% of primary SS patients and in </=10% of the controls. Lymphotoxin beta, as well as a number of major histocompatibility complex genes, cytokines, and lymphocyte activation factors, manifested its role in the pathogenesis of SS. Numerous type I interferon genes related to virus infection were found among the top 200 genes, with increased expression in primary SS. Interestingly, the expression of carbonic anhydrase II, which is essential in saliva production and secretion, and the apoptosis regulator Bcl-2-like 2 were down-regulated in primary SS patients. CONCLUSION: We have identified distinct gene expression profiles in MSGs from patients with primary SS that provide new knowledge about groups of genes that are up-regulated or down-regulated during disease, constituting an excellent platform for forthcoming functional studies.
2013-11-14 | E-MTAB-2073 | biostudies-arrayexpress