Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22007318_1.fastq.gz | Fastqsanger.gz | |||
| SRR22007318_2.fastq.gz | Fastqsanger.gz | |||
| SRR22007319_1.fastq.gz | Fastqsanger.gz | |||
| SRR22007319_2.fastq.gz | Fastqsanger.gz | |||
| SRR22007320_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Transcriptional profiling of mouse retina comparing naïve mouse and experimental autoimmune uveoretinitis (EAU)-developing mouse. EAU was induced by immunization of retinal autoantigens in adjuvants. Retinas were harvested 14 days after immunization.
2010-07-01 | GSE22617 | GEO
Project description:miRNA expression profiling of CD4+ T cells comparing naïve mice and experimental autoimmune uveitis (EAU) mice. EAU was induced by immunization of retinal antigen (IRBP1-20) in complete Freund’s adjuvant (CFA). CD4+ T cells were isolated and purified from the spleen and draining lymph nodes 13 days after immunization.
2022-09-10 | GSE213034 | GEO
Project description:Previous Genome-wide association studies (GWASs) have identified susceptibility loci of primary angle closure glaucoma (PACG), but applicating these findings is difficult. Although shallow anterior chamber depth (ACD) and short axial length (AL) are characteristic phenotypes of PACG, current GWAS variants do not show any correlation with these features, calling for the identification of more risk factors . Here, thicker and enlarged iris was identified as a significant independent risk factors. By employing allelic-specific STARR-seq and assay for transposase-accessible chromatin using sequencing (ATAC-seq), we screened disease-related variants in linkage disequilibrium and identified 2 causative variants in iris. Alterations in these variants may contribute to the pathogenic iris phenotype by upregulating the expression of PLEKHA7 and C10orf53, potentially regulating PACG development and progression. Our efforts nominate the important role of iris and identify pathogenic SNP-target gene interactions for PACG, providing a potentially powerful approach for interpreting noncoding variation of diseases.
2024-07-22 | GSE272247 | GEO
Project description:Background: Blood-retinal barrier cells are known to exhibit a massive phenotypic change during experimental autoimmune uveitis (EAU) development. In an attempt to investigate the mechanisms of blood-retinal barrier (BRB) breakdown at a global level, we studied the gene regulation of total retinal cells and retinal endothelial cells during non-infectious uveitis. Methods: Retinal endothelial cells were isolated by flow cytometry either in Tie2-GFP mice (CD31+ CD45- GFP+ cells), or in wild type C57BL/6 mice (CD31+ CD45- endoglin+ cells). EAU was induced in C57BL/6 mice by adoptive transfer of IRBP1-20-specific T cells. Total retinal cells and retinal endothelial cells from naïve and EAU mice were sorted and their gene expression compared by RNA-Seq. Protein expression of selected genes was validated by immunofluorescence on retinal wholemounts and cryosections and by flow cytometry. Results: Retinal endothelial cell sorting in wild type C57BL/6 mice was validated by comparative transcriptome analysis with retinal endothelial cells sorted from Tie2-GFP mice, which express GFP under the control of the endothelial-specific receptor tyrosine kinase promoter Tie2. RNA-Seq analysis of total retinal cells mainly brought to light upregulation of genes involved in antigen presentation and T cell activation during EAU. Specific transcriptome analysis of retinal endothelial cells allowed us to identify 82 genes modulated in retinal endothelial cells during EAU development. Protein expression of 5 of those genes (serpina3n, lipocalin 2, ackr1, lrg1 and lamc3) was validated at the level of inner BRB cells. Conclusion: Those data not only confirm the involvement of known pathogenic molecules but further provide a list of new candidate genes and pathways possibly implicated in inner BRB breakdown during non-infectious posterior uveitis.
2020-01-28 | GSE144168 | GEO
Project description:We conducted a culture experiment by deeply submerging plants in swine wastewater in culturing Iris tectorum and co-culturing Iris tectorum and Dictyosphaerium sp., and found that the plants grew sub-normal in the plant-microalgae co-culture while the plants were dead after 21 days in the plant culture. We generated a comprehensive RNA-seq dataset from the submerged Iris tectorum leaves in both the plant culture and the plant-microalgae co-culture, aiming at providing information on the response mechanisms of the plants to waterlogging stress. Besides raw reads of the RNA-seq dataset, we used DEseq2 algorithms to detect the differently expressed genes in the plants between the different cultures. Additionally, we performed the plant disease resistance gene analysis for all the differentially expressed genes.
2018-11-03 | GSE122095 | GEO
Project description:Experimental autoimmune uveitis (EAU) in Lewis rats is a model for the clinical heterogeneity of human uveitis. The autoantigens inducing disease in the rat are also seen in human disease. Depending upon the specific autoantigen used, the experimental disease course can be either monophasic or relapsing/remitting and appears to be dictated by the T cell effector phenotype elicited. We investigated potential differences between monophasic and relapsing/remitting effector T cells using transcriptomic profiling and pathway analysis. RNA samples isolated from three independent T cell lines derived from each specificity where analyzed by microarrays. Microarray data was used to obtain transcriptomic changes reflecting signal transduction pathway dysregulation. Keywords: Two group comparison Comparison of two types of cell lines of two different antigen specificities.
2010-12-01 | E-GEOD-19652 | biostudies-arrayexpress
Project description:Tuberculosis Immune Reconstitution Inflammatory Syndrome (TB-IRIS) frequently complicates combined anti-retroviral therapy (ART) and anti-tubercular therapy in HIV-1 co-infected tuberculosis (TB) patients. The immunopathological mechanism underlying TB-IRIS is incompletely defined. Differential transcript abundance in PBMC from IRIS and control patients stimulated with heat killed H37Rv was determined by microarray Blood samples were collected during longitudinal observational studies of TB-IRIS patients and controls (both groups HIV-infected patients placed on antiretroviral treatment). PBMC were stimulated with heat killed H37Rv and RNA extracted.
2013-06-24 | E-GEOD-48237 | biostudies-arrayexpress
Project description:Patients with HIV-associated TB are known to experience systemic hyperinflammation, clinically known as immune reconstitution inflammatory syndrome (IRIS), following the commencement of antiretroviral therapy (ART). No prognostic markers or biomarkers have been identified to date and little is known about the mechanism mediating the hyperinflammation. We recruited a prospective cohort of 63 patients with HIV-associated TB, 33 of whom developed TB-IRIS. Of which transcriptomic profiling was performed using longitudinal whole blood RNA samples from 15 non-IRIS and 17 TB-IRIS patients. Transcriptomic signatures that distinguish patients who would eventually develop IRIS were identified as early as week 0.5 (2-5 days post-ART) and predicted a downstream activation of proinflammatory cytokines. At the peak of IRIS (week 2), transcriptomic signatures were overrepresented by innate receptor signaling pathways including toll-like receptor, IL-1 receptor and TREM-1.
2015-10-05 | GSE58411 | GEO
Project description:Dysregulation of Th17 differentiation was implicated in multiple inflammatory and autoimmune diseases including autoimmune uveitis. In the current study, we have provided evidence indicating that lactate-derived lactylation plays important roles in regulating Th17 differentiation. The lactylation level of CD4+ T cells was upregulated in EAU mice and inhibiting lactylation resulted in impaired EAU progression. We characterized the global lactylome of CD4+ T cells of normal and EAU mice. We found that the differentially lactylated proteins were enriched in pathways related to immune responses including leukocyte differentiation. Importantly, our results show that the lactylation level of Ikzf1 (K164) functions in regulating Th17 differentiation by differentially modulating gene expression patterns which are related to CD4+ T cell differentiation by CUT& Tag analysis. In view of the above mentioned well-documented evidence, Ikzf1 lactylation might represent an important regulator for Th17 differentiation in autoimmune uveitis.
2023-08-28 | GSE226678 | GEO