Evidence map›Paper›PMID 30515838›Full record

ArticleAllergy2019

IL-27 signaling deficiency develops Th17-enhanced Th2-dominant inflammation in murine allergic conjunctivitis model.

Xin Chen, Ruzhi Deng, Wei Chi, Xia Hua, Fan Lu, Fang Bian, Ning Gao, Zhijie Li, Stephen C Pflugfelder, Cintia S de Paiva and 1 more

Open access · greenAbstract read
In one paragraph

Article in Allergy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. IL-27-DependentInternational journal of molecular sciences · 2026
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  19. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
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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

11 authors at 3 institutions in 2 countries.

Xin ChenSchool of Optometry and Ophthalmology, Wenzhou Medical University, Wenzhou, China.
Ruzhi DengSchool of Optometry and Ophthalmology, Wenzhou Medical University, Wenzhou, China.
Wei ChiOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
Xia HuaOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
Fan LuSchool of Optometry and Ophthalmology, Wenzhou Medical University, Wenzhou, China.
Fang BianOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
Ning GaoOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
Zhijie LiDepartment of Pediatrics, Baylor College of Medicine, Houston, Texas.
Stephen C PflugfelderOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
Cintia S de PaivaOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.
De-Quan LiOcular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas.ORCID 0000-0001-9449-4686
Baylor College of Medicine · USSun Yat-sen University · CNWenzhou Medical University · CN

Funding

VISION RESEARCH CENTERP30EY002520 · NEI · BAYLOR COLLEGE OF MEDICINE · PI Samuel M Wu · 1985 to 2026
$14.8M
PATHOGENESIS OF CONJUNCTIVAL SQUAMOUS METAPLASIAR01EY011915 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PFLUGFELDER, STEPHEN C · 1997 to 2023
$8.0M
TLR4-DEPENDENT INNATE IMMUNITY IN POLLEN-TRIGGERED OCULAR ALLERGIC INFLAMMATIONR01EY023598 · NEI · BAYLOR COLLEGE OF MEDICINE · PI LI, DE-QUAN · 2014 to 2018
$2.1M
NEI NIH HHS P30 EY002520NEI NIH HHS R01 EY011915NEI NIH HHS R01 EY023598Oshman FoundationResearch to Prevent BlindnessWilliam Stamps Farish Fund
6 · The paper itself

Abstract

backgroundWhile most studies focus on pro-allergic cytokines, the protective role of immunosuppressive cytokines in allergic inflammation is not well elucidated. This study was to explore a novel anti-inflammatory role and cellular/molecular mechanism of IL-27 in allergic inflammation.

methodsA murine model of experimental allergic conjunctivitis (EAC) was induced in BALB/c, C57BL/6 or IL-27Rα-deficient (WSX-1

resultsTypical allergic manifestations and stimulated thymic stromal lymphopoietin (TSLP) signaling and Th2 responses were observed in ocular surface of EAC models in BALB/c and C57BL/6 mice. The decrease of IL-27 at mRNA (IL-27/EBI3) and protein levels were detected in serum, conjunctiva and CLN, as evaluated by RT-qPCR, immunofluorescent staining, ELISA and Western blotting. EAC induced in WSX-1

conclusionThese findings demonstrated a natural protective mechanism by IL-27, of which signaling deficiency develops a Th17-type hyperresponse that further aggravates Th2-dominant allergic inflammation.

Indexed as

Disease SusceptibilitySignal TransductionAnimalsBiomarkersBiopsyConjunctivitis, AllergicCytokinesDisease Models, AnimalImmunohistochemistryInflammation MediatorsInterleukin-27MiceMice, KnockoutTh17 CellsTh2 CellsT-Lymphocyte SubsetsBiomarkersCytokinesInflammation MediatorsInterleukin-27allergyanti-inflammatory cytokineIL-27Th17Th2

Identifiers

PMID30515838
PMCPMC7190079
OpenAlexW2902823395

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.