Evidence map›Paper›PMID 18425213›Full record

ReviewPLoS pathogens2008

Parallels between pathogens and gluten peptides in celiac sprue.

Michael T Bethune, Chaitan Khosla

Open access · goldAbstract readReview
In one paragraph

Review in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Statement onEFSA journal. European Food Safety Authority · 2021
    Article
  8. Review
  9. Genetic and Environmental Contributors for Celiac Disease.Current allergy and asthma reports · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Oral enzyme therapy for celiac sprue.Methods in enzymology · 2012
    Article
  16. Immune development and intestinal microbiota in celiac disease.Clinical & developmental immunology · 2012
    Review
  17. Article
  18. Article
  19. Anti-microbial antibodies in celiac disease: trick or treat?World journal of gastroenterology · 2009
    Article
  20. 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.

Michael T BethuneDepartment of Biochemistry at Stanford University, Stanford, California, United States of America.
Chaitan Khosla
Stanford University · US

Funding

Role of Transglutaminase 2 in Celiac SprueR01DK063158 · NIDDK · STANFORD UNIVERSITY · PI CHAITAN KHOSLA · 2003 to 2026
$11.2M
NIDDK NIH HHS R01 DK063158
6 · The paper itself

Abstract

Pathogens are exogenous agents capable of causing disease in susceptible organisms. In celiac sprue, a disease triggered by partially hydrolyzed gluten peptides in the small intestine, the offending immunotoxins cannot replicate, but otherwise have many hallmarks of classical pathogens. First, dietary gluten and its peptide metabolites are ubiquitous components of the modern diet, yet only a small, genetically susceptible fraction of the human population contracts celiac sprue. Second, immunotoxic gluten peptides have certain unusual structural features that allow them to survive the harsh proteolytic conditions of the gastrointestinal tract and thereby interact extensively with the mucosal lining of the small intestine. Third, they invade across epithelial barriers intact to access the underlying gut-associated lymphoid tissue. Fourth, they possess recognition sequences for selective modification by an endogenous enzyme, transglutaminase 2, allowing for in situ activation to a more immunotoxic form via host subversion. Fifth, they precipitate a T cell-mediated immune reaction comprising both innate and adaptive responses that causes chronic inflammation of the small intestine. Sixth, complete elimination of immunotoxic gluten peptides from the celiac diet results in remission, whereas reintroduction of gluten in the diet causes relapse. Therefore, in analogy with antibiotics, orally administered proteases that reduce the host's exposure to the immunotoxin by accelerating gluten peptide destruction have considerable therapeutic potential. Last but not least, notwithstanding the power of in vitro methods to reconstitute the essence of the immune response to gluten in a celiac patient, animal models for the disease, while elusive, are likely to yield fundamentally new systems-level insights.

Indexed as

Immunity, InnateAdaptation, PhysiologicalAnimalsBase SequenceCeliac DiseaseDisease Models, AnimalGenetic Predisposition to DiseaseGlutensHumansImmunotoxinsIntestinal MucosaIntestine, SmallLymphoid TissueMolecular Sequence DataPeptidesGlutensImmunotoxinsPeptides

Identifiers

PMID18425213
PMCPMC2323203
OpenAlexW2098645643

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.