Evidence map›Paper›PMID 20689406›Full record

ReviewCurrent opinion in allergy and clinical immunology2010

High-risk corneal allografts and why they lose their immune privilege.

Jerry Y Niederkorn

Abstract readReview
In one paragraph

Review in Current opinion in allergy and clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. "Corneal Nerves, CD11cFrontiers in immunology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. The Eye Sees Eye to Eye With the Immune System: The 2019 Proctor Lecture.Investigative ophthalmology & visual science · 2019
    Article
  17. Article
  18. Observational
  19. Immune Privilege and Eye-Derived T-Regulatory Cells.Journal of immunology research · 2018
    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

1 author.

Jerry Y NiederkornDepartment of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. jerry.niederkorn@utsouthwestern.edu

Funding

THE IMMUNOBIOLOGY OF CORNEAL ALLOGRAFTSR01EY007641 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI NIEDERKORN, JERRY · 1988 to 2016
$5.6M
NEI NIH HHS EY007641NEI NIH HHS R01 EY007641
6 · The paper itself

Abstract

purpose of reviewCorneal allografts are routinely performed without HLA typing or systemic immunosuppressive drugs. However, certain conditions create high risks for immune rejection. This review discusses recent insights into the mechanisms that rob the corneal allograft of its immune privilege. RECENT

findingsStudies in mice have revealed that stimuli that induce new blood vessel growth in the cornea also elicit proliferation of lymph vessels. Lymph vessels facilitate migration of antigen-presenting cells to regional lymph nodes in which they induce alloimmune responses. The presence of blood vessels in the corneal graft bed creates a unique chemokine milieu that stimulates recruitment of sensitized lymphocytes into the corneal allograft. Other data indicate that although corneal allograft survival is closely associated with Foxp3 expression in CD4+CD25+Foxp3+ T regulatory cells (Tregs), reduced expression of Foxp3 in Tregs creates a high risk for graft rejection. Recent evidence indicates that allergic diseases have a profound impact on the immune response and produce a dramatic increase in corneal allograft rejection. SUMMARY: Understanding the underlying mechanisms that create 'high-risk' hosts may provide important therapeutic targets for restoring immune privilege of corneal allografts and enhancing their survival.

Indexed as

Corneal TransplantationAnimalsForkhead Transcription FactorsGraft RejectionHumansHypersensitivityImmune ToleranceInflammationMiceNeovascularization, PathologicRisk FactorsTransplantation, HomologousForkhead Transcription FactorsFOXP3 protein, human

Identifiers

PMID20689406
PMCPMC3116237

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Registered trials

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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.