Evidence map›Paper›PMID 41680338›Full record

ArticleJapanese journal of ophthalmology2026

Conjunctival allergic inflammation involving the interleukin-23/T helper type 17 immune axis in an experimental allergic conjunctivitis mouse model.

Rumi Adachi, Jun Shoji, Noriko Inada, Akiko Tomioka, Satoru Yamagami

Abstract read
In one paragraph

Article in Japanese journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Rumi AdachiDivision of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamichou, Itabashi-ku, Tokyo, 173-8610, Japan.
Jun ShojiDivision of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamichou, Itabashi-ku, Tokyo, 173-8610, Japan.
Noriko InadaDivision of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamichou, Itabashi-ku, Tokyo, 173-8610, Japan.
Akiko TomiokaDivision of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamichou, Itabashi-ku, Tokyo, 173-8610, Japan.
Satoru YamagamiDivision of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamichou, Itabashi-ku, Tokyo, 173-8610, Japan. yamagami.satoru@nihon-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the role of the interleukin-23 (IL-23)/T helper type 17 (Th17) immune axis in conjunctival allergic inflammation using a murine model of experimental allergic conjunctivitis (EAC). STUDY

designExperimental study.

methodsBALB/c mice were assigned to four groups: control (untreated), allergy (EAC), IL-23 (EAC with IL-23 eyelid injection), and non-sensitized IL-23 (non-sensitized with IL-23 eyelid injection). Conjunctival tissue was analyzed histologically to quantify eosinophil and neutrophil infiltration. Gene expression of mRNA in conjunctival tissue was assessed using a PCR array and quantitative RT-PCR.

resultsEosinophilic and neutrophilic infiltration in the subconjunctival tissue was more pronounced in the IL-23 group than in the allergy and control groups. PCR array and quantitative RT-PCR analyses revealed significantly elevated Ccl17/Tarc mRNA expression in the IL-23 group compared to the allergy group. IL-17A mRNA, undetectable in the allergy group, was expressed in the IL-23 group. Additionally, PCR array comparisons between the IL-23 and non-sensitized IL-23 groups showed a significant increase in Rorc and Il1r1 expression in the IL-23 group. At the same time, Mmp3, Ccl7, and Ccr2 were significantly upregulated in the non-sensitized IL-23 group. RT-PCR analysis also demonstrated higher IL-17A mRNA levels in the non-sensitized IL-23 group than in the IL-23 group.

conclusionIL-23 induces mixed eosinophilic-neutrophilic inflammation in conjunctival tissue, characterized by enhanced Th2 and weak Th17 responses in a murine model of EAC. These findings suggest a modulatory role of the IL-23/Th17 axis in influencing the severity and phenotype of allergic conjunctival inflammation.

Indexed as

ConjunctivaConjunctivitis, AllergicGene Expression RegulationInterleukin-23Th17 CellsAnimalsDisease Models, AnimalEosinophilsFemaleMiceMice, Inbred BALB CReal-Time Polymerase Chain ReactionRNA, MessengerInterleukin-23RNA, MessengerAllergic conjunctivitisEosinophil infiltrationExperimental mouse modelInterleukin-23T helper 17 cells

Identifiers

PMID41680338
PMCPMC13452855

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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.