ReviewImmunogenetics2010
Celiac disease: how complicated can it get?
Review in Immunogenetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 159 citations in OpenAlex.
- Classical celiac disease is more frequent with a double dose of HLA-DQB1*02: A systematic review with meta-analysis.PloS one · 2019Pooled it
- HLA-DQ genetics in children with celiac disease: a meta-analysis suggesting a two-step genetic screening procedure starting with HLA-DQ β chains.Pediatric research · 2018Pooled it
- The frequency and characteristics of ultra-short celiac disease in children: A single-center experience.European journal of pediatrics · 2026Article
- The long noncoding RNA lnc13 restrains inflammatory responses to maintain oral tolerance to gluten.Nature immunology · 2026Article
- Microbial transglutaminase in food biotechnology: from biochemical mechanisms to industrial applications.Applied microbiology and biotechnology · 2026Review
- Ultra-short celiac disease in children: histological and autoimmune features.European journal of pediatrics · 2026Article
- Diagnosing celiac disease in children using oral manifestations.BMC gastroenterology · 2024Article
- Prevalence of delivery mode in an Italian nationwide cohort with celiac disease: a SIGENP multicenter retrospective study (the CD-deliver-IT).Italian journal of pediatrics · 2024Article
- Article
- Dimethyl Fumarate and Intestine: From Main Suspect to Potential Ally against Gut Disorders.International journal of molecular sciences · 2023Review
- NK cells contribute to reovirus-induced IFN responses and loss of tolerance to dietary antigen.JCI insight · 2022Article
- Possible relationship between refractory celiac disease and malignancies.World journal of clinical oncology · 2022Review
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
- The expansion of CD14+ CD163+ subpopulation of monocytes and myeloid cells-associated cytokine imbalance; candidate diagnostic biomarkers for celiac disease (CD).Journal of clinical laboratory analysis · 2021Article
- Emergence of Celiac disease and Gluten-related disorders in Asia.Journal of neurogastroenterology and motility · 2021Review
- Article
- Article
- Diagnosing coeliac disease: Out with the old and in with the new?World journal of gastroenterology · 2020Review
- Stimulatory Response of Celiac Disease Peripheral Blood Mononuclear Cells Induced by RNAi Wheat Lines Differing in Grain Protein Composition.Nutrients · 2019Article
- Observational
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4(+) T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4(+) T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.
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What OpenQuestion holds
Registered trials
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.