Evidence map›Paper›PMID 18799120›Full record

ArticleCurrent gastroenterology reports2008

Immunopathogenesis of celiac disease.

Jason Tye-Din, Robert Anderson

Abstract read
PubMed Publisher
In one paragraph

Article in Current gastroenterology reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.5field-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

7 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Article
  3. Oral microbiome: possible harbinger for children's health.International journal of oral science · 2020
    Review
  4. Article
  5. Review
  6. Salivary microbiota and metabolome associated with celiac disease.Applied and environmental microbiology · 2014
    Article
  7. Article
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

2 authors at 1 institution in 1 country.

Jason Tye-DinAutoimmunity and Transplantation Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, Australia.
Robert Anderson
Walter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celiac disease is a chronic inflammatory disease caused by dietary gluten that affects 1% of Europeans and North Americans. Gluten is unusual because it is consumed in relatively large amounts, is partially resistant to luminal digestion in the human small intestine, and when absorbed, is susceptible to post-translational modification (deamidation) by mucosal transglutaminase. Deamidation of certain gluten peptides enhances their binding to HLA-DQ2 or HLA-DQ8 and creates neodeterminants capable of stimulating CD4+ T cells. Only 5% of individuals with HLA-DQ2 and 0.5% of those with HLA-DQ8 have celiac disease, so immuno-logic tolerance to gluten is the norm. The critical steps in the immunopathogenesis of celiac disease are broadly understood, but little is known regarding mechanisms of tolerance to gluten. The effectiveness of therapies being developed for celiac disease will test the accuracy of our current understanding of disease pathogenesis.

Indexed as

Celiac DiseaseHumans

Identifiers

PMID18799120
OpenAlexW2023238740

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.