Evidence map›Paper›PMID 25563498›Full record

ArticleMucosal immunology2015

Suppression of Toll-like receptor-mediated innate immune responses at the ocular surface by the membrane-associated mucins MUC1 and MUC16.

B B Menon, C Kaiser-Marko, S Spurr-Michaud, A S Tisdale, I K Gipson

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Inflammatory Response of Presbyopes Neophyte Contact Lens Wearers during 6 Months of Multifocal Lens Wear.Ophthalmic & physiological optics : the journal of the British College of Ophthalmic Opticians (Optometrists) · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Ocular surface glycocalyx in health and disease.Frontiers in cell and developmental biology · 2025
    Review
  8. Review
  9. Article
  10. MUC16: clinical targets with great potential.Clinical and experimental medicine · 2024
    Review
  11. Article
  12. Review
  13. Animal Models in Eye Research: Focus on Corneal Pathologies.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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 at 2 institutions in 1 country.

B B MenonSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
C Kaiser-MarkoSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
S Spurr-MichaudSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
A S TisdaleSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
I K GipsonSchepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA.
Smith-Kettlewell Eye Research Institute · USMassachusetts Eye and Ear Infirmary · US

Funding

MUCINS OF THE OCULAR SURFACER01EY003306 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI GIPSON, ILENE K. · 1985 to 2015
$8.9M
Bacteria-Mucin Interactions at the Ocular SurfaceR01EY018850 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI GIPSON, ILENE K. · 2009 to 2012
$1.9M
NEI NIH HHS R01 EY003306NEI NIH HHS R01 EY018850NEI NIH HHS R01EY018850
6 · The paper itself

Abstract

Membrane-associated mucins (MAMs) expressed on the ocular surface epithelium form a dense glycocalyx that is hypothesized to protect the cornea and conjunctiva from external insult. In this study, the hypothesis that the MAMs MUC1 and MUC16, expressed on the apical surface of the corneal epithelium, suppress Toll-like receptor (TLR)-mediated innate immune responses was tested. Using an in vitro model of corneal epithelial cells that are cultured to express MAMs, we show that reduced expression of either MUC1 or MUC16 correlates with increased message and secreted protein levels of the proinflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF-α) following exposure of cells to the TLR2 and TLR5 agonists, heat-killed Listeria monocytogenes and flagellin, respectively. As mice express Muc1 (but not Muc16) in the corneal epithelium, a Muc1(-/-) mouse model was used to extend in vitro findings. Indeed, IL-6 and TNF-α message levels were increased in the corneal epithelium of Muc1(-/-) mice, in comparison with wild-type mice, following exposure of enucleated eyes to the TLR2 and TLR5 agonists. Our results suggest that the MAMs MUC1 and MUC16 contribute to the maintenance of immune homeostasis at the ocular surface by limiting TLR-mediated innate immune responses.

Indexed as

Immunity, InnateAnimalsCA-125 AntigenCell Line, TransformedConjunctivaCorneaCytokinesHumansListeria monocytogenesMembrane ProteinsMiceMice, KnockoutMucin-1Toll-Like Receptor 2Toll-Like Receptor 5CA-125 AntigenCytokinesMembrane ProteinsMUC16 protein, humanMUC16 protein, mouseMUC1 protein, humanmuc1 protein, mouseMucin-1TLR2 protein, humanTlr2 protein, mouseTLR5 protein, humanToll-Like Receptor 2Toll-Like Receptor 5

Identifiers

PMID25563498
PMCPMC4495011
OpenAlexW1990775561

What OpenQuestion holds

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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.