Evidence map›Paper›PMID 22660791›Full record

ReviewSeminars in immunopathology2012

Intraepithelial lymphocytes in celiac disease immunopathology.

Valérie Abadie, Valentina Discepolo, Bana Jabri

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 180 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Dietary gluten triggers concomitant activation of CD4+ and CD8+ αβ T cells and γδ T cells in celiac disease.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  4. Article
  5. Review
  6. GPR55 negatively regulates CD8Journal of molecular histology · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Assessment of Intraepithelial Lymphocytes Count in Potential Celiac Disease.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

46 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 3 countries.

Valérie AbadieSainte-Justine Hospital Research Centre, Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Montreal, QC, H3T 1C5, Canada. valerie.abadie@umontreal.ca
Valentina Discepolo
Bana Jabri
University of Chicago · USUniversité de Montréal · CA

Funding

ULTRASTRUCTURE AND CYTOMORPHOLOGY COREP30DK042086 · NIDDK · UNIVERSITY OF CHICAGO · PI LIU, CAMBRIAN YANGSHAO · 1990 to 2025
$29.8M
Innate and adaptive immunity in celiac diseaseR01DK067180 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2005 to 2024
$8.5M
Regulation of normal human IEL by NKG2D and IL-15R01DK058727 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2001 to 2010
$2.7M
NIDDK NIH HHS DK058727NIDDK NIH HHS DK42086NIDDK NIH HHS R01 DK67180
6 · The paper itself

Abstract

Celiac disease is a T cell-mediated immune disorder induced by dietary gluten that is characterized by the development of an inflammatory anti-gluten CD4 T cell response, anti-gluten antibodies, and autoantibodies against tissue transglutaminase 2 and the activation of intraepithelial lymphocytes (IELs) leading to the destruction of the intestinal epithelium. Intraepithelial lymphocytes represent a heterogeneous population of T cells composed mainly of cytotoxic CD8 T cells residing within the epithelial layer, whose main role is to maintain the integrity of the epithelium by eliminating infected cells and promoting epithelial repair. Dysregulated activation of IELs is a hallmark of CD and is critically involved in epithelial cell destruction and the subsequent development of villous atrophy. In this review, we compare and contrast the phenotype and function of human and mouse small intestinal IELs under physiological conditions. Furthermore, we discuss how conditions of epithelial distress associated with overexpression of IL-15 and non-classical MHC class I molecules induce cytotoxic IELs to become licensed killer cells that upregulate activating NKG2D and CD94/NKG2C natural killer receptors, acquiring lymphokine killer activity. Pathways leading to dysregulated IEL activation could eventually be targeted to prevent villous atrophy and treat patients who respond poorly to gluten-free diet.

Indexed as

AnimalsCeliac DiseaseHomeostasisHumansIntestinal MucosaIntestine, SmallLymphocytesProtein Glutamine gamma Glutamyltransferase 2Protein Glutamine gamma Glutamyltransferase 2

Identifiers

PMID22660791
OpenAlexW2084159240

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.