Evidence map›Paper›PMID 26690299›Full record

ArticleClinical and experimental immunology2016

Desiccating stress-induced disruption of ocular surface immune tolerance drives dry eye disease.

M Guzmán, I Keitelman, F Sabbione, A S Trevani, M N Giordano, J G Galletti

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  8. Article
  9. Animal Models in Eye Research: Focus on Corneal Pathologies.International journal of molecular sciences · 2023
    Review
  10. Effects of Cathepsin S Inhibition in the Age-Related Dry Eye Phenotype.Investigative ophthalmology & visual science · 2023
    Article
  11. Article
  12. Article
  13. Ocular surface immune cell diversity in dry eye disease.Indian journal of ophthalmology · 2023
    Review
  14. Review
  15. The Effects of Fisetin on Cyclosporine-Treated Dry Eye Disease in Dogs.International journal of molecular sciences · 2023
    Article
  16. Dry Eye Disease: What Is the Role of Vitamin D?International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

M GuzmánImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
I KeitelmanImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
F SabbioneImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
A S TrevaniImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
M N GiordanoImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
J G GallettiImmunology Laboratory, Institute of Experimental Medicine, National Academy of Medicine/CONICET, Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dry eye is an allegedly autoimmune disorder for which the initiating mechanisms and the targeted antigens in the ocular surface are not known, yet there is extensive evidence that a localized T helper type 1 (Th1)/Th17 effector T cell response is responsible for its pathogenesis. In this work, we explore the reconciling hypothesis that desiccating stress, which is usually considered an exacerbating factor, could actually be sufficient to skew the ocular surface's mucosal response to any antigen and therefore drive the disease. Using a mouse model of dry eye, we found that desiccating stress causes a nuclear factor kappa B (NF-κB)- and time-dependent disruption of the ocular surface's immune tolerance to exogenous ovalbumin. This pathogenic event is mediated by increased Th1 and Th17 T cells and reduced regulatory T cells in the draining lymph nodes. Conversely, topical NF-κB inhibitors reduced corneal epithelial damage and interleukin (IL)-1β and IL-6 levels in the ocular surface of mice under desiccating stress. The observed effect was mediated by an augmented regulatory T cell response, a finding that highlights the role of mucosal tolerance disruption in dry eye pathogenesis. Remarkably, the NF-κB pathway is also involved in mucosal tolerance disruption in other ocular surface disorders. Together, these results suggest that targeting of mucosal NF-κB activation could have therapeutic potential in dry eye.

Indexed as

AnimalsCell LineDisease Models, AnimalDry Eye SyndromesEpithelium, CornealImmune ToleranceInterleukin-1betaInterleukin-6Lymph NodesLymphocyte CountMiceMice, Inbred BALB CMice, Inbred C3HNF-kappa BOvalbuminStress, PhysiologicalIL1B protein, mouseInterleukin-1betaInterleukin-6NF-kappa BOvalbuminconjunctival tolerancedesiccating stressdry eyemucosal toleranceocular surface

Identifiers

PMID26690299
PMCPMC4837231
OpenAlexW2218643654

What OpenQuestion holds

Textmetadata
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.