Evidence map›Paper›PMID 19538307›Full record

ReviewAnnals of the New York Academy of Sciences2009

Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms.

Jeroen Visser, Jan Rozing, Anna Sapone, Karen Lammers, Alessio Fasano

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 2 pooled it
10.7field-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

107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 235 citations in OpenAlex.

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  14. Environmental health perspectives · 2024
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  19. Polysaccharide fromInternational journal of molecular sciences · 2022
    Article
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47 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

5 authors at 2 institutions in 2 countries.

Jeroen VisserDepartment of Cell Biology, Section Immunology and Histology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Jan Rozing
Anna Sapone
Karen Lammers
Alessio Fasano
University of Maryland, Baltimore · USUniversity of Groningen · NL

Funding

Zot, Zonulin, and Pathophysiology of Intestinal Tight JunctionsR01DK048373 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI FASANO, ALESSIO · 1996 to 2015
$4.4M
Timing of Gluten Intake In Infant Nutrition and Risk of Celiac Disease AutoimmuniR21DK078699 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI FASANO, ALESSIO · 2008 to 2009
$413k
NIDDK NIH HHS DK-078699NIDDK NIH HHS DK-48373NIDDK NIH HHS R01 DK048373NIDDK NIH HHS R21 DK078699
6 · The paper itself

Abstract

Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on celiac disease (CD), an autoimmune enteropathy, and type 1 diabetes (T1D), a hyperglycosaemia caused by a destructive autoimmune process targeting the insulin-producing pancreatic islet cells. Even if environmental factors and genetic susceptibility are clearly involved in the pathogenesis of autoimmunity, for most autoimmune disorders there is no or little knowledge about the causing agent or genetic makeup underlying the disease. In this respect, CD represents a unique autoimmune disorder because a close genetic association with HLA-DQ2 or HLA-DQ8 haplotypes and, more importantly, the environmental trigger (the gliadin fraction of gluten-containing grains wheat, barley, and rye) are known. Conversely, the trigger for autoimmune destruction of pancreatic ss cells in T1D is unclear. Interestingly, recent data suggest that gliadin is also involved in the pathogenesis of T1D. There is growing evidence that increased intestinal permeability plays a pathogenic role in various autoimmune diseases including CD and T1D. Therefore, we hypothesize that besides genetic and environmental factors, loss of intestinal barrier function is necessary to develop autoimmunity. In this review, each of these components will be briefly reviewed.

Indexed as

AutoimmunityAnimalsCeliac DiseaseCell Membrane PermeabilityCholera ToxinDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseGliadinHaplotypesHaptoglobinsHLA-DQ AntigensHumansIntestinal MucosaModels, BiologicalProtein PrecursorsTight JunctionsCholera ToxinGliadinHaptoglobinsHLA-DQ AntigensProtein Precursorszonulin

Identifiers

PMID19538307
PMCPMC2886850
OpenAlexW2124038080

What OpenQuestion holds

Textmetadata
LicenceTDM
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.