Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16821700_1.fastq.gz | Fastqsanger.gz | |||
| SRR16821700_2.fastq.gz | Fastqsanger.gz | |||
| SRR16821701_1.fastq.gz | Fastqsanger.gz | |||
| SRR16821701_2.fastq.gz | Fastqsanger.gz | |||
| SRR16821602_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Background and Aims: Celiac disease (CeD) is an autoimmune disease triggered by dietary gluten in genetically predisposed individuals. Deamidation of gluten peptides by the CeD autoantigen and enzyme transglutaminase 2 (TG2) is central to the pathogenesis of CeD. Inhibition of TG2 with the specific inhibitor ZED1227 effectively prevents gluten-induced histological damage in CeD patients. Here we aimed to explore the blood DNA methylomic changes in ZED1227-treated CeD patients undergoing a gluten challenge. Results: Drug treatment revealed consistent patterns suggesting normalization of the DNA methylome indicating that ZED1227 attenuated the systemic responses to gluten challenge. Conclusions: These findings provide evidence that ZED1227 can significantly prevent the gluten-induced CeD-associated systemic changes. Clinical trial: EudraCT 2017-002241-30
2026-06-18 | GSE319777 | GEO
Project description:Dietary gluten proteins (prolamins) from wheat, rye, and barley are the driving forces behind celiac disease, an organ-specific autoimmune disorder that targets both the small intestine and organs outside the gut. In the small intestine, gluten induces inflammation and a typical morphological change of villous atrophy and crypt hyperplasia. Gut lesions improve and heal when gluten is excluded from the diet and the disease relapses when patients consume gluten. Oral immune tolerance towards gluten may be kept for years or decades before breaking tolerance in genetically susceptible individuals. Celiac disease provides a unique opportunity to study autoimmunity and the transition in immune cells as gluten breaks oral tolerance. Seventy-three celiac disease patients on a long-term gluten-free diet ingested a known amount of gluten daily for six weeks. A peripheral blood sample and intestinal biopsies were taken before and six weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus height to crypt depth ratio to quantify gluten-induced gut mucosal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained or broke oral tolerance in the face of a gluten challenge.
2017-01-27 | GSE87629 | GEO
Project description:Coeliac disease is a small intestinal disorder caused by an abarrent immune response towards dietary gluten due to activation of pro-inflammatory gluten specific CD4+ T cells. Histological evaluation and classification of gluten induced musosal changes is part of the diagnostic work up. of adults. The kinetics of mucosal recovery following commencesment of a gluten free diet (disease remission) and the degree of mucosal changes induced by gluten reintroduction (gluten challenge) varies between patients. Also, patients classified with similar clinical and histological disease remission, can develop different degree of mucosal damage following the same gluten challenge regime. This variation poses a challenge for the interpretation of gluten induced mucosal changes both in a diagnostic and clinical trial settings. In this study, we have analysed material from small intestinal biopsies collected from 19 treated coeliac disease patients before and after completion of a 14-day oral gluten challenge. These patients are part of a previoslpreviouslyu described study where all patients were in clinical and mucosal remission at baseline but only some patients developed histological changes in the mucosa in response to gluten. We have performed shotgun LC-MSMS analysis and label-free quantification of total gut tissue and from laser capture microdissected epithelial cell layer samples. We found that differences in tissue proteome expression could separate patients as responders and non-responders to the gluten challenge. Patients whoich responded strongly to gluten , had signs of gut inflammation already at baseline, supported by presence of low-level blood inflammatory parameters and a slight increase in numbers of gluten-specific CD4+ T cells at baseline. Our proteomics analysis demonstrated baseline differences in gut tissue state between patients that were not evident from routine clinical and histological evaluation. These baseline differences likely explains why some patients respond more strongly to gluten challenge than others.
2021-03-03 | PXD018977 | Pride
Project description:Chronic inflammation driven by persistent antigenic challenge with dietary gluten permanently reshapes the tissue-resident TCRgd+ intraepithelial lymphocyte compartment in patients with celiac disease.
2018-12-12 | GSE123649 | GEO
Project description:Objective Development of novel treatments for coeliac disease (CeD) is dependent on precise tools to monitor changes in gluten-induced mucosal damage. Current histology measures are subjective and difficult to standardise. Biopsy proteome scoring is an objective alternative to histology which is based on robust changes in biological pathways that directly reflect gluten-induced mucosal damage. In this study we aimed to evaluate biopsy proteome scoring as effect measure in a clinical trial setting by measuring intestinal remodeling in response to oral gluten challenge. Design We analyzed biopsies from a gluten challenge trial of treated CeD patients that consumed 3 g (n=6) or 10 g (n=7) gluten per day for 14 days. Sections from individually embedded biopsies collected before and after challenge were processed for proteome scoring (n = 109) and measurement of Vh:Cd ratio (n = 58). Proteome scores were compared to histology, intraepithelial lymphocyte (IEL) frequency and plasma interleukin-2 (IL-2). Results Change in proteome scores were significant for the group of patients who consumed 10 g gluten, but not for the group who consumed 3 g gluten. Altogether, 8 of 13 patients had changes in delta proteome scores above cut-off. Proteome scores correlated with Vh:Cd ratios both at run-in and at day 15. Proteome scores at day 15 correlated with IEL frequency and with serum IL-2 levels measured 4 hours post gluten intake. Conclusion Biopsy proteome scoring is a simple and reliable measure of gluten-induced mucosal remodeling in response to 14-day oral gluten challenge.
2025-04-08 | PXD050655 | Pride
Project description:Gluten reactive T-cells from blood samples from patients undergoing a 3 day gluten challenge. Samples were collected on day 6.
Both gluten reactive and non-gluten reactive T-cells were sequenced.
| EGAD00001006899 | EGA
Project description:Individuals with celiac disease (CeD) on a long-term gluten-free diet (GFD) underwent a 6-week gluten challenge combined with 100mg per day of the transglutaminase 2 enzyme -inhibitor, ZED1227 (PGCd, n = 28) or placebo (PGCp, n = 19). The samples were collected at baseline (GFD) and post-gluten challenge (PGC). Mass spectrometry-based lipidomic and proteomics profiling, along with genome-wide DNA methylation analysis, were applied to plasma samples obtained from 47 CeD patients. Comparative analyses were performed between the groups, with adjustment for BMI, age, sex, and country of origin.
2026-06-15 | PXD069597 | Pride
Project description:Single cell and bulk TCR sequences - gluten challenge study
| PRJNA377207 | ENA
Project description:Here is reported the first study of transcriptome analyses using the Illumina HiSeq 4000 platform for three kinds of wheat (G represents Strong gluten wheat, Z represents middle gluten wheat,R represents weak gluten wheat). The variation of wheat varieties with different gluten content is mainly shown in the content of gluten, flour is divided into high gluten powder ( > 30%), medium gluten powder (26%-30%) and low gluten powder ( < 20%), according to the wet gluten content. In total, over 102.6 Gb clean reads were produced and 114, 621 unigenes were assembled; more than 59,085 unigenes had at least one significant match to an existing gene model. Differentially expressed gene analysis identified 2339 and 2600 unigenes which were expressed higher or lower among strong gluten, middle gluten and weak gluten wheat. After functional annotation and classification, three dominant pathways including protein isomerase, antioxidase activity and energy metabolism, and 410 unigenes related to gluten strength polymerization of wheat were discovered. In strong-gluten wheat, low molecular weight subunit content is higher than weak-gluten wheat, and the activity of cysteine synthase and isomerase is increased, which may promote the cross-linking of low molecular weight protein to high molecular weight protein. Meanwhile, POD enzyme strengthens gluten network and CAT enzyme affects gluten polymerization, along with higher ATPase activity, which will provides energy for protein polymerization reaction in comparison of strong-gluten wheat and weak-gluten wheat. The accuracy of these RNA-seq data was validated by qRT-PCR analysis. These data will extend our knowledge of quality characteristics of wheat and provide a theoretical foundation for molecular mechanism research of wheat.
2020-09-03 | GSE122699 | GEO
Project description:Gluten-specific CD4+ T cells are drivers of celiac disease (CeD). Here we aimed to characterize such cells in blood of treated CeD patients during gluten challenge with comparison to similar cells of untreated disease.
Treated CeD patients underwent a 3-day gluten-challenge with blood sampling at baseline and day 6 (d6). Blood cells were stained with HLA-DQ:gluten tetramers (Tetramer). CD4+, gut-homing Tetramer+ and Tetramer- effector-memory T (TEM) cells at d6 were subjected to bulk RNA-seq (n=7).
| EGAS00001004988 | EGA