Evidence map›Paper›PMID 16682498›Full record

ArticleThe Journal of experimental medicine2006

Reprogramming of CTLs into natural killer-like cells in celiac disease.

Bertrand Meresse, Shane A Curran, Cezary Ciszewski, Gerasim Orbelyan, Mala Setty, Govind Bhagat, Leanne Lee, Maria Tretiakova, Carol Semrad, Emily Kistner and 7 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

141 citing papers in PubMed, 304 citations in OpenAlex.

  1. Trial
  2. 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
  3. Article
  4. T cell receptors for antigen on intraepithelial cytolytic T lymphocytes in celiac disease engage enterocyte HLA-E and HLA-B.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Intraepithelial Lymphocytes of the Intestine.Annual review of immunology · 2024
    Review
  16. Review
  17. Review
  18. Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

81 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

17 authors at 6 institutions in 2 countries.

Bertrand MeresseDepartment of Pathology, University of Chicago, Chicago, IL 60637, USA.
Shane A Curran
Cezary Ciszewski
Gerasim Orbelyan
Mala Setty
Govind Bhagat
Leanne Lee
Maria Tretiakova
Carol Semrad
Emily Kistner
Robert J Winchester
Veronique Braud
Lewis L Lanier
Daniel E Geraghty
Peter H Green
Stefano Guandalini
Bana Jabri
Pediatrics and Genetics · USCentre National de la Recherche Scientifique · FRColumbia University · USFred Hutch Cancer Center · USUniversity of California, San Francisco · USUniversity of Chicago · US

Funding

Role of Transglutaminase 2 in Celiac SprueR01DK063158 · NIDDK · STANFORD UNIVERSITY · PI CHAITAN KHOSLA · 2003 to 2026
$11.2M
Regulation of normal human IEL by NKG2D and IL-15R01DK058727 · NIDDK · UNIVERSITY OF CHICAGO · PI JABRI, BANA · 2001 to 2010
$2.7M
NK CELL RECEPTORS AND THEIR LIGANDSR01CA089294 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI LANIER, LEWIS L · 2001 to 2005
$1.6M
NCI NIH HHS R01 CA089294NCI NIH HHS R01 CA89294NIDDK NIH HHS R01 DK058727NIDDK NIH HHS R01 DK063158NIDDK NIH HHS R01 DK58727
6 · The paper itself

Abstract

Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon gamma-producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases.

Indexed as

Cell ProliferationBase SequenceCeliac DiseaseCell DifferentiationChronic DiseaseCytomegalovirus InfectionsGene Expression ProfilingGene Expression RegulationHumansInterferon-gammaIntestinal MucosaIntestine, SmallKiller Cells, NaturalLymphomaMolecular Sequence DataPhosphorylationInterferon-gammaReceptors, ImmunologicZAP70 protein, humanZAP-70 Protein-Tyrosine Kinase

Identifiers

PMID16682498
PMCPMC2121214
OpenAlexW2128452798

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.