Evidence map›Paper›PMID 28051088›Full record

ArticleMucosal immunology2017

Lacrimal gland-derived IL-22 regulates IL-17-mediated ocular mucosal inflammation.

Y W Ji, S K Mittal, H S Hwang, E-J Chang, J H Lee, Y Seo, A Yeo, H Noh, H S Lee, S K Chauhan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2017. 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
4.0field-weighted citation impact, top 7% 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, 40 citations in OpenAlex.

  1. Review
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  3. CD4Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Interleukin-22 Influences the Th1/Th17 Axis.Frontiers in immunology · 2021
    Review
  16. Article
  17. Article
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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 4 institutions in 2 countries.

Y W JiInstitute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
S K MittalSchepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA.
H S HwangDepartment of Ophthalmology, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon, Korea.
E-J ChangSchepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA.
J H LeeMyunggok Eye Research Institute, Kim's Eye Hospital, Konyang University College of Medicine, Seoul, Korea.
Y SeoInstitute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
A YeoInstitute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
H NohInstitute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
H S LeeBiostatistics Collaboration Unit, Medical Research Center, Yonsei University College of Medicine, Seoul. Korea.
S K ChauhanSchepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA.
H K LeeInstitute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
Yonsei University · KRMassachusetts Eye and Ear Infirmary · USHallym University · KRKonyang University · KR

Funding

Ocular Immune Regulation by Mesenchymal Stem CellsR01EY024602 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI CHAUHAN, SUNIL K · 2015 to 2025
$6.5M
NEI NIH HHS R01 EY024602
6 · The paper itself

Abstract

Inflammatory damage of mucosal surface of the eye is a hallmark of dry eye disease (DED) and, in severe cases, can lead to significant discomfort, visual impairment, and blindness. DED is a multifactorial autoimmune disorder with a largely unknown pathogenesis. Using a cross-sectional patient study and a well-characterized murine model of DED, herein we investigated the immunoregulatory function of interleukin-22 (IL-22) in the pathogenesis of DED. We found that IL-22 levels were elevated in lacrimal fluids of DED patients and inversely correlated with severity of disease. Acinar cells of the lacrimal glands (LGs), not inflammatory immune cells, are the primary source of IL-22, which suppresses inflammation in ocular surface epithelial cells upon desiccating stress. Moreover, loss of function analyses using IL-22 knockout mice demonstrated that IL-22 is essential for suppression of ocular surface infiltration of Th17 cells and inhibition of DED induction. Our novel findings elucidate immunoregulatory function of LG-derived IL-22 in inhibiting IL-17-mediated ocular surface epitheliopathy in DED thus making IL-22 a new relevant therapeutic target.

Indexed as

Acinar CellsAdultAgedAnimalsCross-Sectional StudiesDry Eye SyndromesEyeFemaleHumansInterleukin-17Interleukin-22InterleukinsLacrimal ApparatusMaleMiceMice, Inbred C57BLInterleukin-17Interleukin-22Interleukins

Identifiers

PMID28051088
PMCPMC5496813
OpenAlexW2568094208

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.