Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

40380f5a-350e-44bc-9f8f-97bc9f527d4c - samples

ABSTRACT: Paired T-cell receptor sequences sequenced from single cells, from intraepithalial CD8+ ÃŽÂ±ÃŽÂ² T-cells. Sequences are from from untreated and treated (on a gluten-free diet) celiac disease patients and controls.

PROVIDER: EGAD00001006900 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Single-cell T-cell receptor sequencing of intraepithelial CD8+ ÃŽÂ±ÃŽÂ² T-cells in celiac disease

Project description:Single-cell paired TCR sequencing of intraepithelial CD8+ ÃŽÂ±ÃŽÂ² T-cells in gluten-free diet treated and untreated celiac disease patients and in controls. (Paired end, amplicon sequencing).

| EGAS00001004989 | EGA

Single-cell T-cell receptor sequencing of intraepithelial gammadelta T-cells in celiac disease

Project description:Single-cell paired TCR sequencing of intraepithelial ÃŽÂ³ÃŽÂ´ T-cells in gluten-free diet treated and untreated celiac disease patients and in controls. (Paired end, amplicon sequencing).

| EGAS00001003897 | EGA

Gluten induces rapid reprogramming of natural memory αβ and γδ intraepithelial T cells to induce cytotoxicity in celiac disease

Project description:Celiac disease (CD) is an autoimmune disease in which intestinal inflammation is induced by dietary gluten. The means through which gluten-specific CD4+T cell activation culminates in intraepithelial T cell (T-IEL)–mediated intestinal damage remain unclear. Here, we performed multiplexed single-cell analysis of intestinal and gluten-induced peripheral blood T cells from patients in different CD states and healthy controls. Untreated, active, and potential CD were associated with an enrichment of activated intestinal T cell populations, including CD4+follicular T helper (TFH) cells, regulatory T cells (Tregs), and natural CD8+αβ and γδ T-IELs. Natural CD8+αβ and γδ T-IELs expressing activating natural killer cell receptors (NKRs) exhibited a distinct TCR repertoire in CD and persisted in patients on a gluten-free diet without intestinal inflammation. Our data further show that NKR-expressing cytotoxic cells, which appear to mediate intestinal damage in CD, arise from a distinct NKR-expressing memory population of T-IELs. After gluten ingestion, both αβ and γδ T cell clones from this memory population of T-IELs circulated systemically along with gluten-specific CD4+T cells and assumed a cytotoxic and activating NKR-expressing phenotype. Collectively, these findings suggest that cytotoxic T cells in CD are rapidly mobilized in parallel with gluten-specific CD4+T cells after gluten ingestion.

2024-01-13 | GSE252762 | GEO

Genome-wide analysis of B and T cell gene expression during a six-week gluten challenge in patients with celiac disease

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

Transcription profiling of duodenum biopsies from patients with celiac disease taken at time of diagnosis or after two years of a gluten free diet

Project description:Study on the effects of long term, dietary, consumption of gliadin (gluten) in patients with celiac disease. Comparison of expression profiles of biopsies from normalized patients treated with gluten-free diet >2 years (FU-follow-up samples) versus biopsies from patients with active disease (Dx-at diagnosis samples)

2009-06-01 | E-MEXP-1828 | biostudies-arrayexpress

dca23f3c-c32b-4ecd-9def-aef945f90182 - samples

Project description:In order to characterize the T cell receptor (TCR) repertoire of gluten specific T cells, we performed high-throughput DNA sequencing of rearranged TCR-ÃŽÂ± and TCR-ÃŽÂ² genes of the single HLA-DQ2.5:DQ2.5-gluten tetramer binding CD4+ T cells isolated from blood, biopsies and T cell line from celiac disease patients.

| EGAD00001006977 | EGA

Single cell transcriptomic analysis of the immune cell compartment in the human small intestine and in Celiac disease

Project description:Celiac disease is an autoimmune disorder in which ingestion of dietary gluten triggers an immune reaction in the small intestine leading to destruction of the lining epithelium. Current treatment focusses on lifelong adherence to a gluten-free diet. Gluten-specific CD4+ T cells and cytotoxic intraepithelial CD8+ T cells have been proposed to be central in disease pathogenesis. Here we use unbiased single-cell RNA-sequencing and explore the heterogeneity of CD45+ immune cells in the human small intestine. We show altered myeloid cell transcriptomes present in active celiac lesions. CD4+ and CD8+ T cells transcriptomes show extensive changes and we define a natural intraepithelial lymphocyte population that is reduced in celiac disease. We show that the immune landscape in Celiac patients on a gluten-free diet is only partially restored compared to control samples. Altogether, we provide a single cell transcriptome resource that can inform the immune landscape of the small intestine during Celiac disease.

| EGAS00001003751 | EGA

Transcription profiling by array of human duodenum biopsies from normalized celiac patients treated with gliadin

Project description:Study of the effects of re-exposure to gliadin of intestinal biopsies from normalized celiac patients (>2 years on gluten free diet). Comparison of the expresson profile in biopsy portions incubated with 10ug/ml gliadin versus without gliadin for 4 hours.

2009-06-01 | E-MEXP-1823 | biostudies-arrayexpress

Reprogramming of CTLs into natural killer-like cells in celiac disease

Project description:Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon g–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases. Keywords: NKG2C; LAK; CTL; NK receptor; IEL; Mucosal Immunity; Celiac Disease

2006-05-15 | GSE4592 | GEO

Novel type of EATL evolving from mucosal M-NM-3M-NM-4-T-cells in a RCD type I patient

Project description:Enteropathy associated T-cell lymphoma (EATL) is a rare non-Hodgkin lymphoma that may complicate celiac disease and typically occurs in patients with refractoriness to the gluten- free diet. The majority of these patients harbor intra-epithelial lymphocytes (IEL) with an aberrant phenotype in the small intestine which are thus considered as the M-bM-^@M-^XprecursorM-bM-^@M-^Y lymphoma cells. We here report on a case of extra-intestinal EATL that originated from a clonal M-NM-3M-NM-4-IEL population rather than from aberrant IEL. This EATL displayed a distinctive pattern of immunophenotypical, T-cell receptor immunogenetic, and chromosomal aberrancies defining this lymphoma as a novel variant of EATL. sample vs reference

2014-04-02 | E-GEOD-56425 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data