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Gene expression assessed by genome wide hybridization bead array in intestinal epithelial cells (IECs) isolated from small intestinal biopsies of celiac disease patients with active disease and clinical controls

ABSTRACT: Analysis of role of small intestinal epithelial cells (IECs) in the immunopathology of celiac disease

ORGANISM(S): Homo sapiens

PROVIDER: GSE102991 | GEO | 2017/08/24

SECONDARY ACCESSION(S): PRJNA399709

REPOSITORIES: GEO

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Gene expression assessed by genome wide hybridization bead array in intraepithelial lymphocytes (IELs) isolated from small intestinal biopsies of celiac disease patients with active disease and clinical controls

Project description:Analysis of role of small intestinal intraepithelial lymphocytes (IELs) in the immunopathology of celiac disease

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Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria [CTR 32 33 34]

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Project description:Celiac disease is a chronic immune-mediated disorder with an important genetic component. To date, there are 57 independent association signals from 39 non-HLA loci, and a total of 66 candidate genes have been proposed. We aimed to scrutinize the functional implication of 45 of those genes by analyzing their expression in the disease tissue of celiac patients (at diagnosis/treatment) compared to non-celiac controls. The sample set consisted of 15 CD children at diagnosis (on a gluten-containing diet, with CD associated antibodies, atrophy of intestinal villi and crypt hyperplasia), and the same patients in remission after being treated with GFD for >2 years (asymptomatic, antibody negative, and normalized intestinal epithelium at that time), plus 15 tissue samples from non-celiac individuals not suffering from inflammation at the time of endoscopy used as controls

2014-09-30 | E-GEOD-61849 | 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

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Expression analysis in intestinal mucosa of genes under association peaks in celiac disease

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RNA sequencing derived from intestinal biopsies from healthy controls and celiac disease patients

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2021-02-16 | GSE146190 | GEO

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