Evidence map›Paper›PMID 26856700›Full record

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

Regulation of Adenosine Deaminase on Induced Mouse Experimental Autoimmune Uveitis.

Dongchun Liang, Aijun Zuo, Ronglan Zhao, Hui Shao, Henry J Kaplan, Deming Sun

Erratum issuedOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
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. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Dongchun LiangDoheny Eye Institute, Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90033;
Aijun ZuoDoheny Eye Institute, Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90033;
Ronglan ZhaoDoheny Eye Institute, Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90033; Department of Medical Laboratory, Key Laboratory of Clinical Laboratory Diagnostics, University of Shandong, Weifang Medical University, Weifang, Shandong 261053, China; and.ORCID http://orcid.org/0000-0002-4302-2563
Hui ShaoDepartment of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville, Louisville, KY 40202.
Henry J KaplanDepartment of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville, Louisville, KY 40202.
Deming SunDoheny Eye Institute, Department of Ophthalmology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90033; dsun@doheny.org.ORCID http://orcid.org/0000-0003-4851-0416
University of California, Los Angeles · USUniversity of Louisville · USWeifang Medical University · CN

Funding

Role of IL-17+ Autoreactive T Cells in Experimental Autoimmune Uveitis (EAU)R01EY018827 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 2009 to 2023
$4.8M
Regulation by Gammadelta T Cells of Autoimmune Uveitis (EAU)R01EY022403 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 2012 to 2015
$1.6M
NEI NIH HHS EY0022403NEI NIH HHS EY018827NEI NIH HHS R01 EY018827NEI NIH HHS R01 EY022403
6 · The paper itself

Abstract

Adenosine is an important regulator of the immune response, and adenosine deaminase (ADA) inhibits this regulatory effect by converting adenosine into functionally inactive molecules. Studies showed that adenosine receptor agonists can be anti- or proinflammatory. Clarification of the mechanisms that cause these opposing effects should provide a better guide for therapeutic intervention. In this study, we investigated the effect of ADA on the development of experimental autoimmune uveitis (EAU) induced by immunizing EAU-prone mice with a known uveitogenic peptide, IRBP1-20. Our results showed that the effective time to administer a single dose of ADA to suppress induction of EAU was 8-14 d postimmunization, shortly before EAU expression; however, ADA treatment at other time points exacerbated disease. ADA preferentially inhibited Th17 responses, and this effect was γδ T cell dependent. Our results demonstrated that the existing immune status strongly influences the anti- or proinflammatory effects of ADA. Our observations should help to improve the design of ADA- and adenosine receptor-targeted therapies.

Indexed as

Adenosine DeaminaseAnimalsAutoimmune DiseasesCells, CulturedEye ProteinsFemaleHumansImmunizationImmunologic FactorsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalMolecular Targeted TherapyPeptide FragmentsReceptors, Antigen, T-Cell, gamma-deltaAdenosine DeaminaseEye ProteinsImmunologic FactorsPeptide FragmentsReceptors, Antigen, T-Cell, gamma-deltaRetinol-Binding ProteinsRetinol-Binding Proteins, Interstitial

Identifiers

PMID26856700
PMCPMC4779687
OpenAlexW2253090357

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.