Evidence map›Paper›PMID 27263022›Full record

ReviewClinical reviews in allergy & immunology2019

Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review.

Tiina Rauhavirta, Minna Hietikko, Teea Salmi, Katri Lindfors

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. [Role of HLA genetic variants in autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  2. Review
  3. Article
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  6. Preclinical evaluation of anEJNMMI radiopharmacy and chemistry · 2024
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  10. The Impact ofInternational journal of molecular sciences · 2023
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  12. Review
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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

4 authors at 3 institutions in 1 country.

Tiina RauhavirtaPediatric Research Center, University of Tampere and Tampere University Hospital, Finn Medi 3, 33520, Tampere, Finland.
Minna HietikkoPediatric Research Center, University of Tampere and Tampere University Hospital, Finn Medi 3, 33520, Tampere, Finland.
Teea SalmiSchool of Medicine, University of Tampere, Tampere, Finland.
Katri LindforsPediatric Research Center, University of Tampere and Tampere University Hospital, Finn Medi 3, 33520, Tampere, Finland. katri.lindfors@uta.fi.
FinnMedi (Finland) · FITampere University · FITampere University · FI

Funding

Competitive State Research Financing of the Expert Responsibility Areas of Tampere University Hospital 9T058
6 · The paper itself

Abstract

Celiac disease is a common inflammatory disorder with a prevalence of 1-2 % in which a distinct dietary wheat, rye, and barley component, gluten, induces small-bowel mucosal villous atrophy, crypt hyperplasia, and inflammation. The small-bowel mucosal damage can be reversed by a strict lifelong gluten-free diet, which is currently the only effective treatment for the condition. A key player in the pathogenetic process leading to the enteropathy is played by a protein called transglutaminase 2 (TG2), which is able to enzymatically modify gluten-derived gliadin peptides. The TG2-catalyzed deamidation of the gliadin peptides results in their increased binding affinity to the disease-predisposing human leukocyte antigen (HLA) DQ2 and DQ8 molecules, thus enabling a strong immune response to be launched. Blocking the enzymatic activity of TG2 has thus been suggested as a suitable novel pharmacological approach to treat celiac disease. By virtue of its transamidation capacity, TG2 is also able to cross-link gliadin peptides to itself, this resulting in the generation of TG2-gliadin peptide complexes whose presence might provide an explanation for the generation of the TG2 autoantibodies characteristic of celiac disease. Due to their excellent specificity for the disorder, the TG2-targeted autoantibodies are widely used in the diagnostics as a first-line test to select patients for gastrointestinal endoscopy. More recently, it has come to be appreciated that these autoantibodies and also the TG2-specific B cells might play an active role in the disease pathogenesis. In this review, we assess the role of TG2, TG2-specific B cells, and autoantibodies in celiac disease.

Indexed as

AdultAnimalsAutoantibodiesAutoimmune DiseasesB-LymphocytesCeliac DiseaseChildDiet, Gluten-FreeFemaleGliadinGTP-Binding ProteinsHLA-DQ AntigensHumansMaleMiceMiddle AgedAutoantibodiesGliadinGTP-Binding ProteinsHLA-DQ2 antigenHLA-DQ8 antigenHLA-DQ AntigensProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesCeliac diseaseTransglutaminase 2Transglutaminase 2 autoantibodies

Identifiers

PMID27263022
OpenAlexW2410123544

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.