Evidence map›Paper›PMID 26643477›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Cutting Edge: IL-1 Receptor Signaling is Critical for the Development of Autoimmune Uveitis.

Chi-Keung Wan, Chang He, Lin Sun, Charles E Egwuagu, Warren J Leonard

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  12. Immune Privilege: The Microbiome and Uveitis.Frontiers in immunology · 2020
    Review
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  19. Observational
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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

5 authors at 1 institution in 1 country.

Chi-Keung WanLaboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.
Chang HeMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.ORCID http://orcid.org/0000-0003-1178-5950
Lin SunMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
Charles E EgwuaguMolecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 wjl@helix.nih.gov egwuaguc@nei.nih.gov.ORCID http://orcid.org/0000-0002-9986-3839
Warren J LeonardLaboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and wjl@helix.nih.gov egwuaguc@nei.nih.gov.
National Institutes of Health · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
IL-2 Family Cytokines and their Receptors-- Biology of the IL-21 systemZIAHL005408 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LEONARD, WARREN J · 2009 to 2025
$23.7M
DNA Sequencing Core (DSC)ZICHL006058 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHU, JUN · 2010 to 2016
$16.6M
Mechanisms of immune homeostasis and regulation of intraocular inflammationZIAEY000372 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$6.5M
Regulation of JAK/STAT pathways in the eyeZIAEY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$5.4M
Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

IL-1β is a proinflammatory cytokine important for local and systemic immunity. However, aberrant production of this cytokine is implicated in pathogenic mechanisms of a number of inflammatory diseases, including Behçet's disease and age-related macular degeneration. In this study, we report the increased secretion of IL-1β in the retina by neutrophils, macrophages, and dendritic cells during ocular inflammation and show that loss of IL-1R signaling confers protection from experimental autoimmune uveitis. Moreover, the amelioration of experimental autoimmune uveitis in Il1r-deficient mice was associated with reduced infiltration of inflammatory cells into the retina and decreased numbers of uveitogenic Th17 cells that mediate uveitis. These findings indicate the possible utility of IL-1R-blocking agents for the treatment of ocular inflammatory diseases.

Indexed as

Signal TransductionAnimalsAutoimmune DiseasesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFlow CytometryInterleukin-1betaMiceMice, Inbred C57BLMice, KnockoutReceptors, Interleukin-1UveitisInterleukin-1betaReceptors, Interleukin-1

Identifiers

PMID26643477
PMCPMC4707108
OpenAlexW2193532480

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.