Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell transcriptomic analysis of retinal immune regulation and blood-retinal barrier function during experimental autoimmune uveitis

ABSTRACT: Single-cell transcriptomic analysis of retinal immune regulation and blood-retinal barrier function during experimental autoimmune uveitis

PROVIDER: PRJNA1009136 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25759400_1.fastq.gz	Fastqsanger.gz
	SRR25759400_2.fastq.gz	Fastqsanger.gz
	SRR25759401_1.fastq.gz	Fastqsanger.gz
	SRR25759401_2.fastq.gz	Fastqsanger.gz
	SRR25759402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

Single-cell transcriptomic analysis of retinal immune regulation and blood-retinal barrier function during experimental autoimmune uveitis

Project description:Uveitis is characterised by breakdown of the blood-retinal barrier (BRB), allowing infiltration of immune cells that mediate intraocular inflammation, which can lead to irreversible damage of the neuroretina and the loss of sight. Treatment of uveitis relies heavily on corticosteroids and systemic immunosuppression due to limited understanding of the molecular immune interactions that underpin ocular immune homeostasis. By performing single-cell transcriptomic analysis of whole dissociated mouse retinas with experimental autoimmune uveitis (EAU) versus healthy control, we gained an unbiased appreciation of the immune interactions that drive retinal inflammation in a model of posterior uveitis.

2024-08-29 | GSE241700 | GEO

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

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

Murine CD4+ T cells: naive vs. experimental autoimmune uveitis

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

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

Project description:Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

| PRJNA602922 | ENA

Murine CD4+ T cells: naive vs. experimental autoimmune uveitis

Project description:Murine CD4+ T cells: naive vs. experimental autoimmune uveitis

| PRJNA878815 | ENA

Effector T cells driving monophasic vs relapse/remitting experimental autoimmune uveitis show unique pathway signatures

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

Effector T cells driving monophasic vs relapse/remitting experimental autoimmune uveitis show unique pathway signatures

2010-12-01 | GSE19652 | GEO

Single-Cell transcriptional profiling reveals immune dysregulation and abnormal immune-inflammatory communications between immune and retinal cells in uveitis

Project description:Uveitis is an immune-inflammatory disease that can cause blindness. However, little is known about a comprehensive atlas of the ocular cellular and inflammatory components in uveitis. Here, single-cell RNA sequencing was performed to construct a transcriptomic atlas of ocular cells from experimental autoimmune uveitis (EAU) and control mice to identify disease- associated immune cell subsets and molecules. We reveal 15 cell types in eyes and found an α-Synuclein positive microglia subset and plasma cell subset with high level of cytokines. The heterogeneous plasma cells subsets communicated with DC, T cells and retinal cells via various cytokines and molecular pairing. The G protein Rab1A participated in the inflammatory response of plasma cells. Altogether, we revealed the heterogeneous inflammatory genes, EAU-specific immune cell populations, and dysregulated communications of immune and retinal cells in EAU. This result provides a systematic view of the transcriptional map of uveitis and a foundation for studying the cellular and molecular mechanisms and pathogenesis of this disease.

2023-07-10 | GSE236389 | GEO

Dysfunction of retinal dopaminergic system exacerbates experimental autoimmune uveoretinitis in Gnat1rd17 mice

Project description:This study investigated the effect of the Gnat1 (rod transducin alpha subunit) gene deficiency in Gnat1rd17 mice on the retinal transcriptome remodeling, and whether this remodeling is protective or maladaptive with regard to photoreceptor damage driven by autoimmune process. The results of this study showed that Gnat1rd17 mice exhibited transcriptomic changes indicative of remodeling in photoreceptor segments and connecting cilium, deregulated inflammatory pathways and dopaminergic signaling, followed by development of exacerbated experimental autoimmune uveoretinitis, which was ameliorated by dopamine replacement. These findings suggest rod transducin alpha subunit a critical modulator of retinal homeostasis and immune response through regulation of retinal dopaminergic system.

2022-01-11 | E-MTAB-10863 | biostudies-arrayexpress

Proteome dynamcis in biobanked horse peripheral blood derived lymphocytes (PBL) with induced autoimmune uveitis

Project description:Equine recurrent uveitis (ERU) is the only spontaneous model for recurrent autoimmune uveitis in humans, where T cells target retinal proteins. Differences between normal and autoaggressive lymphocytes were identified in this study by analyzing peripheral blood derived lymphocytes (PBL) proteomes from the same case with IRBP-induced uveitis sampled before (day 0), during (day 15) and after uveitic attack (day 23). Relative protein abundances of PBL were investigated in a quantitative, label-free differential proteome analysis in cells that were kept frozen for 14 years since the initial experiment. Quantitative data could be acquired for 2632 proteins at all three time-points. Profound changes (> 2 fold change) in PBL protein abundance were observed when comparing day 0 to 15, representing acute inflammation (234 regulated proteins) and day 0 to 23 (cessation; 382 regulated). Significant differences applied to proteins with functions in integrin signaling during active uveitis, involving “Erk and pi-3 kinase are necessary for collagen binding in corneal epithelia”, “Integrins in angiogenesis” and “Integrin-linked kinase signaling” pathways. In contrast, at cessation of uveitic attack, significantly changed proteins belonged to pathways of “nongenotropic androgen signaling”, “classical complement pathway” and “Amb2 integrin signaling”. Several members of respective pathways were earlier shown to be changed in naturally occurring uveitis, underscoring the significance of these findings here and proofing the value of the induced model in mimicking spontaneous autoimmune uveitis.

2017-08-31 | PXD005580 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data