Evidence map›Paper›PMID 39198470›Full record

ArticleScientific reports2024

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

Joel Quinn, Ahmed Salman, Christopher Paluch, Matthew Jackson-Wood, Michelle E McClements, Jian Luo, Simon J Davis, Richard J Cornall, Robert E MacLaren, Calliope A Dendrou and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

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  18. Interferons andFrontiers in immunology · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Joel QuinnNuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Ahmed SalmanNuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Christopher PaluchMiroBio Ltd, Winchester House, Heatley Rd, Oxford, UK.
Matthew Jackson-WoodMiroBio Ltd, Winchester House, Heatley Rd, Oxford, UK.
Michelle E McClementsNuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.ORCID 0000-0002-2941-4464
Jian LuoRespiratory Medicine Unit, Nuffield Department of Medicine, Experimental Medicine, University of Oxford, Oxford, UK.
Simon J DavisRadcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.
Richard J CornallNuffield Department of Medicine, Henry Wellcome Building for Molecular Physiology, University of Oxford, Oxford, UK.
Robert E MacLarenNuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.ORCID 0000-0002-3096-4682
Calliope A DendrouNuffield Department of Medicine, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Kanmin XueNuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. kanmin.xue@eye.ox.ac.uk.ORCID 0000-0003-0065-9131

Funding

Wellcome Trust (Wellcome) 216593/Z/19/Z
6 · The paper itself

Abstract

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 disease pathogenesis. We performed single-cell RNA-sequencing of retinas, as well as bulk RNA-sequencing of retinal pigment epithelial (RPE) cells from mice with experimental autoimmune uveitis (EAU) versus healthy control. This revealed that the Th1/Th17-driven disease induced strong gene expression changes in response to inflammation in rods, cones, Müller glia and RPE. In particular, Müller glia and RPE cells were found to upregulate expression of chemokines, complement factors, leukocyte adhesion molecules and MHC class II, thus highlighting their contributions to immune cell recruitment and antigen presentation at the inner and outer BRB, respectively. Additionally, ligand-receptor interaction analysis with CellPhoneDB revealed key interactions between Müller glia and T cell / natural killer cell subsets via chemokines, galectin-9 to P4HB/TIM-3, PD-L1 to PD-1, and nectin-2/3 to TIGIT signalling axes. Our findings elucidate mechanisms contributing to breakdown of retinal immune privilege during uveitis and identify novel targets for therapeutic interventions.

Indexed as

Autoimmune DiseasesBlood-Retinal BarrierSingle-Cell AnalysisUveitisAnimalsDisease Models, AnimalEpendymoglial CellsGene Expression ProfilingMiceMice, Inbred C57BLRetinaRetinal Pigment EpitheliumTranscriptome

Identifiers

PMID39198470
PMCPMC11358488

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.