Evidence map›Paper›PMID 23667648›Full record

ArticlePloS one2013

Galectin-9-mediated protection from allo-specific T cells as a mechanism of immune privilege of corneal allografts.

Machiko Shimmura-Tomita, Mingcong Wang, Hiroko Taniguchi, Hisaya Akiba, Hideo Yagita, Junko Hori

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023
    Review
  7. Epigenetic Regulation of Corneal Epithelial Differentiation by TET2.International journal of molecular sciences · 2023
    Article
  8. The level of Tim-3+CD8+ T cells can serve as a potential marker for evaluating the severity of acute graft-versus-host disease after haplo-PBSCT.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
    Article
  9. Association ofFrontiers in medicine · 2023
    Article
  10. Review
  11. Article
  12. Galectins as Regulators of Corneal Inflammation.Current opinion in physiology · 2021
    Article
  13. Corneal Allografts: Factors for and against Acceptance.Journal of immunology research · 2021
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. High-risk corneal allografts: A therapeutic challenge.World journal of transplantation · 2016
    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

6 authors at 4 institutions in 1 country.

Machiko Shimmura-TomitaDepartment of Ophthalmology, Nippon Medical School, Tokyo, Japan. machiko@jichi.ac.jp
Mingcong Wang
Hiroko Taniguchi
Hisaya Akiba
Hideo Yagita
Junko Hori
Juntendo University · JPNippon Medical School · JPJichi Medical University · JPNippon Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The eye is an immune-privileged organ, and corneal transplantation is therefore one of the most successful organ transplantation. The immunosuppressive intraocular microenvironment is known as one of the mechanisms underlying immune privilege in the eye. T-cell immunoglobulin and mucin domain (Tim)-3 is a regulatory molecule for T-cell function, and galectin (Gal)-9 is a Tim-3 ligand. We investigated the role of this pathway in establishing the immune-privileged status of corneal allografts in mice. Gal-9 is constitutively expressed on the corneal epithelium, endothelium and iris-ciliary body in normal mouse eyes and eyes bearing surviving allografts, and Tim-3 was expressed on CD8 T cells infiltrating the allografts. Allograft survival in recipients treated with anti-Tim-3 monoclonal antibody (mAb) or anti-Gal-9 mAb was significantly shorter than that in control recipients. In vitro, destruction of corneal endothelial cells by allo-reactive T cells was enhanced when the cornea was pretreated with anti-Gal-9 mAb. Blockade of Tim-3 or Gal-9 did not abolish anterior chamber-associated immune deviation. We propose that constitutive expression of Gal-9 plays an immunosuppressive role in corneal allografts. Gal-9 expressed on corneal endothelial cells protects them from destruction by allo-reactive T cells within the cornea.

Indexed as

Corneal TransplantationAnimalsAnterior ChamberCD8-Positive T-LymphocytesCell DeathCytoprotectionEndothelial CellsEndothelium, CornealGalectinsGraft RejectionGraft SurvivalHepatitis A Virus Cellular Receptor 2ImmunityLymphoid TissueMaleMicegalectin 9, mouseGalectinsHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2Receptors, Virus

Identifiers

PMID23667648
PMCPMC3646846
OpenAlexW2111290903

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.