Transglutaminase 2 at the Interface of Gene Regulation and Antigen Processing in HLA-Restricted Immunity of Celiac Disease.

Faustina Barbara Cannea, Alessandra Padiglia

Abstract readReview

In one paragraph

Review in Genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Faustina Barbara CanneaDepartment of Life and Environmental Sciences (DiSVA), Biomedical Section, University of Cagliari, Cittadella Universitaria di Monserrato, Monserrato, 09042 Cagliari, Italy.

Alessandra PadigliaDepartment of Life and Environmental Sciences (DiSVA), Biomedical Section, University of Cagliari, Cittadella Universitaria di Monserrato, Monserrato, 09042 Cagliari, Italy.ORCID 0000-0002-0540-3082

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celiac disease (CD) is an immune-mediated enteropathy triggered by dietary gluten in genetically predisposed individuals. Although HLA-DQ2 and HLA-DQ8 are the primary genetic determinants of susceptibility, they are not sufficient to explain disease onset and progression. A key molecular event in CD pathogenesis is the post-translational modification of gluten peptides by transglutaminase 2 (TG2), which enhances their binding to HLA-DQ molecules and promotes CD4

Indexed as

Antigen PresentationCeliac DiseaseGTP-Binding ProteinsHLA-DQ AntigensTransglutaminasesGene Expression RegulationGlutensHumansProtein Glutamine gamma Glutamyltransferase 2GlutensGTP-Binding ProteinsHLA-DQ2 antigenHLA-DQ8 antigenHLA-DQ AntigensProtein Glutamine gamma Glutamyltransferase 2Transglutaminasesautoimmunityceliac diseasegene environment interactiongene regulationgluten deamidationHLA-DQ2HLA-DQ8TG2TGM2transglutaminase 2

Identifiers

PMID42195005

DOI10.3390/genes17050548

PMCPMC13206229

What OpenQuestion holds

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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.