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Gastrointestinal symptoms and pathology in patients with Common variable immunodeficiency

ABSTRACT: Based on the findings of increased IEL in duodenal biopsies in CVID, an overlap with celiac disease has been suggested. In the present study, increased IEL, in particular in the pars descendens of the duodenum, was one of the most frequent histopathological finding. We therefore examined the gene expression profile in pars descendens of duodenum in CVID patients with increased IEL (n=13, IEL mean 34 [range 22-56] IEL/100 EC), CVID with normal levels of IEL (n=7), celiac disease (n=10, Marsh grade 3a or above) and healthy controls (n=17) by gene expression microarray GI histopathological findings in 53 CVID patients that underwent upper and lower endoscopic examination were addressed. For the microarray analysis 20 CVID (7 CVID_normal and 13 CVID with incresed IEL), 10 patients with celiac diseases and 17 healthy controls were included.

ORGANISM(S): Homo sapiens

SUBMITTER: Silje Fjellgård Jørgensen

PROVIDER: E-GEOD-72625 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gastrointestinal symptoms and pathology in patients with Common variable immunodeficiency

Project description:Based on the findings of increased IEL in duodenal biopsies in CVID, an overlap with celiac disease has been suggested. In the present study, increased IEL, in particular in the pars descendens of the duodenum, was one of the most frequent histopathological finding. We therefore examined the gene expression profile in pars descendens of duodenum in CVID patients with increased IEL (n=12, IEL mean 34 [range 22-56] IEL/100 EC), CVID with normal levels of IEL (n=8), celiac disease (n=10, Marsh grade 3a or above) and healthy controls (n=17) by gene expression microarray

2015-09-02 | GSE72625 | GEO

Gene expression in duodenal biopsy samples from CVID enteropathy patients and healthy controls

Project description:A subgroup of CVID patients presents with gastrointestinal complications (enteropathy), which manifests in the duodenum as celiac like-diese ase. CVID enteropathy patients can present with severe histopathology in form of villous atrophy (CVID VA) or without VA (CVID noVA). RNAseq data from CVID VA and CVID noVA derived duodenal tissues were compared to each other and to healthy controls.

2023-02-10 | GSE189820 | GEO

Transcriptomic Signature of Celiac show induced epithelial proliferation coupled with suppressed metabolic functions

Project description:Background and aims: Celiac disease is provoked by gluten exposure, but the resultant pathogenic process in the duodenum is not well understood. We aimed to define the core celiac transcriptomic signature and pathologic pathways in pre-treatment diagnostic duodenum biopsies. Methods: We use mRNAseq to define pre-treatment diagnostic duodenum gene expression in 54 pediatric celiac patients and non-celiac controls, and we validate our key findings in an independent cohort of 40 participants. We further define similar and divergent genes and pathways in 177 Crohn disease patients and controls. Results: We observe a marked suppression of mature epithelial metabolic functions in celiac patients, overlapping substantially with the Crohn signature. A marked adaptive immune response was noted for the up-regulated signature including interferon response, alpha-beta, and gamma-delta T-cells that overlapped to some extant with the Crohn signature. However, we identified a celiac specific signature linked to increased cell proliferation, nuclear division, and cell cycle activity that was localized primarily to the epithelia as noted by CCNB1 and Ki67 staining. Lastly, we demonstrate the utility of the transcriptomic date to correctly classify disease or healthy states in the discovery and validation cohorts. Conclusion: Our data provide insights into celiac pathogenesis and can stimulate new approaches to address this highly prevalent condition.

2020-04-10 | GSE131705 | 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

Novel type of EATL evolving from mucosal γδ-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 ‘precursor’ lymphoma cells. We here report on a case of extra-intestinal EATL that originated from a clonal γδ-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.

2014-04-02 | GSE56425 | GEO

Human gut derived-organoids as model to study gluten response and effects of microbiota bioproducts in celiac disease

Project description:Celiac disease (CeD) is an intestinal immune-mediated disorder caused by gluten ingestion in genetically predisposed subjects. CeD is characterized by villous atrophy, altered intestinal permeability, crypt hyperplasia and innate and adaptive immune response. This study aimed to develop and validate the use of intestinal organoids from celiac patients to study CeD. A repository of organoids from duodenum of non-celiac and celiac patients was generated and characterized accordingly to standard procedures. RNA-seq analysis was employed to study the global gene expression program of CeD (n=3) and non-CeD (n=3) organoids sets. While the three celiac derived organoids shared similar transcriptional signatures the NC samples set appeared more heterogeneous. We found 486 genes differentially expressed between the two groups. Of them, 299 genes were downregulated (FC<2; FDR<0.05) and 187 were upregulated in CeD (FC >2; FDR<0.05). We observed CeD organoids had significantly altered expression of genes associated with barrier function, innate immunity, and stem cell function.

2019-05-29 | GSE113492 | GEO

Analysis of expression of genes involved in celiac disease

Project description:Celiac disease (CD) is a chronic immune-mediated disorder with an important genetic component. We analyzed the expression of candidate genes in biopsies from duodenum.

2016-10-31 | GSE84729 | GEO

Expression of candidate genes in Celiac Disease - Associated genes and regulatory elements (part 1)

Project description:Celiac disease is a chronic immune-mediated disorder with an important genetic component. We analyzed the expression of candidate genes and regulatory elements in biopsies from duodenum.

2018-09-28 | GSE87457 | GEO

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

Comparative analysis of chicken Intestinal Intraepithelial lymphocytes (IEL) following Eimeria acervulina (EA), E. maxima (EM), or E. tenella (ET) infection

Project description:Relative expression levels of mRNAs in chicken IEL experimentally infected with EA, EM, or ET were measured at 1 to 6 days post-infection (dpi) following primary and secondary infections. One week-old chickens were uninfected (negative control) or were orally inoculated with sporulated oocysts of EA, EM, or ET. One week later, the infected chickens were challenged with an identical inoculum of the homologous parasite. Intestinal samples were collected daily from 5 birds in a treatment group at from 1 to 6 dpi following primary and secondary infections. Cecum, duodenum, and jejunum were collected from the birds challenged with E. acervulina, E. maxima, and E. tenella, respectively. Uninfected control samples and one of the 3 infection group samples were labeled with different fluorescent dyes and hybridized simultaneously on the same slide using a reference design with a dye swap protocol. Thirty seven-condition experiment, Non-infected control vs. Primary or secondary EA, EM, or ET infected IEL at 1 to 6. Biological replicates: 2 replicates with dye-switching from each infection groups. Two replicates per array.

2011-08-14 | E-GEOD-31213 | biostudies-arrayexpress

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