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Recurrent Campylobacter jejuni and Campylobacter coli infections

ABSTRACT: Two clinical cases of common variable immunodeficiency (CVID) patients with Campylobacters-associated diarrhoea and repeated bacteraemia over a period of almost 10 years

PROVIDER: PRJEB87827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14791210_1.fastq.gz	Fastqsanger.gz
	ERR14791210_2.fastq.gz	Fastqsanger.gz
	ERR14791211_1.fastq.gz	Fastqsanger.gz
	ERR14791211_2.fastq.gz	Fastqsanger.gz
	ERR14791132_1.fastq.gz	Fastqsanger.gz

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Project description:common variable immunodeficiency (CVID)

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Duodenal inflammation in common variable immunodeficiency has altered transcriptional response to viruses

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Duodenal inflammation in Common variable immunodeficiency has altered transcriptional response to viruses

Project description:To elucidate the role of duodenal microenvironment in Common variable immunodeficiency pathogenesis (CVID), we sought to explore the transcriptome regulation in duodenal biopsies.

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Transcriptomic analysis of follicular CD8 T cells in human secondary lymphoid organs in healthy donors and patients with common variable immunodeficiency

Project description:We performed a comparison of transcriptome between follicular CD8 T cells (CXCR5+CD8+CD3+) from 3 lymph nodes of patients with common variable immunodeficiency (CVID) and 3 tonsils of healthy donors, discovering 67 differentially expressed genes that show immunoregulatory potential of CVID follicular CD8 T cells.

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Multi-omics Analysis of naive B cells of patients harboring the C104R mutation in TACI

Project description:Common variable immunodeficiency (CVID) is the most prevalent form of symptomatic primary immunodeficiency in humans. The genetic cause of CVID is still unknown in about 70% of cases. 10% of CVID patients carry heterozygous mutations in the tumor necrosis factor receptor superfamily member 13B gene (TNFRSF13B), encoding TACI. Mutations in TNFRSF13B alone may not be sufficient for the development of CVID, as 1% of the healthy population carry these mutations. The common hypothesis is that TACI mutations are not fully penetrant and additional factors contribute to the development of CVID. To determine these additional factors, we investigated the perturbations of transcription factor (TF) binding and the transcriptome profiles in unstimulated and CD40L/IL21-stimulated naïve B cells from CVID patients harboring the C104R mutation in TNFRSF13B and compared them to their healthy relatives with the same mutation. In addition, the proteome of stimulated naïve B cells was investigated. For functional validation, intracellular protein concentrations were measured by flow cytometry. Our analysis revealed 8% less accessible chromatin in unstimulated naïve B cells and 25 % less accessible chromatin in class-switched memory B cells from affected and unaffected TACI mutation carriers compared to healthy donors. The most enriched TF binding motifs in TACI mutation carriers involved members from the ETS, IRF and NF-B TF families. Validation experiments supported dysregulation of the NF-B and MAPK pathways. In steady state, naïve B cells had increased cell death pathways and reduced cell metabolism pathways; while after stimulation, enhanced immune responses and decreased cell survival was detected. Using a multi-omics approach, our findings provide valuable insights into the impaired biology of naïve B cells from TACI mutation carriers.

2022-10-14 | PXD035459 | Pride

EGAS00001004489-2-sc-2022-02-17T14:43:00Z - samples

Project description:Common variable immunodeficiency (CVID) is the most prevalent primary immunodeficiency. Here the authors perform single cell omics analyses in CVID discordant monozygotic twins and show epigenetic and transcriptional alterations associated with activation in memory B cells.

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IgM from common variable immunodeficiency patients narrowly recognizes erythrocyte and platelet glycans

Project description:Autoantibody-mediated cytopenias (AICs) regularly occur in profoundly IgG-deficient common variable immunodeficiency (CVID) patients. The isotypes, antigenic targets, and origin(s) of disease-causing autoantibodies in this patient population are unclear. Herein, we report that erythrocytes and platelets from CVID patients with AICs (CVID+AIC) are coated with autoreactive IgM. Glycan array-based analyses of CVID+AIC plasma IgM revealed narrow reactivities to erythrocytic I/i antigens and platelet expressed I/i antigen-related glycans but starkly lower binding to hundreds of other pathogen and tumor-associated carbohydrates. Polyclonal B-cell receptors with corresponding I/i antigen reactivities were highly enriched among CVID+AIC circulating marginal zone (MZ) B cells. Within secondary lymphoid tissues, MZ B cells secreted copious IgM when activated by IL-10 secreting FOXP3-CD25hiTfh cells. In lymph nodes from immunocompetent controls, MZ B cells localized outside of GCs near rare FOXP3-CD25+ cells and plentiful FOXP3+ regulatory T cells. In CVID+AIC lymph nodes, counterpart cells localized to similar anatomic positions but CD25hiTfh cells greatly outnumbered regulatory T cells. In total, our findings indicate glycan-reactive IgM autoantibodies produced outside of GC borders may contribute to the autoimmune pathogenesis of CVID.

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Project description:The homeostasis of circulating B cell subsets in the peripheral blood of healthy adults is well regulated, but in disease it can be severely disturbed. Thus, a subgroup of patients with common variable immunodeficiency (CVID) presents with an extraordinary expansion of an unusual B cell population characterized by the low expression of CD21. Since these circulating atypical B cells in the blood of CVID patients could not be assigned to any certain B cell differentiation stage in the periphery, they were designated as CD21low B cells. Although, CD21low B cells are polyclonal and unmutated IgM+IgD+ B cells like naive B cells in the peripheral blood, they reveal several distinct phenotypic and functional features. In order to uncover the the global programme of gene expression underlying these differences and changes in CD21low B cells we have performed microarray hybridization experiments and identified differentially expressed genes which define a distinct gene expression profile in CD21low B cells compared to naive B cells. Leucocytes were separated by Ficoll gradient from peripheral blood of healthy donors (HD) and CVID patients. CD19+CD27-CD38+CD21+ naive B cells of HD as well as naive and CD19hiCD27-CD38lowCD21low (CD21low) B cells of CVID patients were sorted using a MoFlow cell sorter. RNA was extracted from sorted ex vivo B cell subpopulations and hybridized on Affymetrix microarrays. Gene expression profiles were compared between CD21low B cells and naive B cells of CVID patients as well as HD naive B cells.

2009-07-30 | E-GEOD-17269 | biostudies-arrayexpress

Gene signature of regulatory T cells isolated from children with Selective IgA Deficiency and Common Variable Immunodeficiency.

Project description:In our study we aimed to analyze the gene expression profile of Treg cells in CVID and SIgAD patients, compared to age-matched healthy controls. Selective IgA deficiency (SIgAD) is the most common and common variable immunodeficiency (CVID) is the most symptomatic form of predominant antibody deficiency. Despite differences in the clinical picture, a similar genetic background is suggested. A common feature of both disorders is the occurrence of autoimmune conditions. Regulatory T cells (Tregs) are the major immune cell type that maintains autoimmune tolerance. As the different types of abnormalities of Treg cells were associated with autoimmune disorders in primary immunodeficiency (PID) patients, in our study we aimed to analyze the gene expression profile of Treg cells in CVID and SIgAD patients, compared to age-matched healthy controls. The transcriptome-wide gene profiling was performed using microarray technology. As a results, we analyzed and visualized global expression patterns of genes and pathways of isolated population of Treg cells. We showed the differences at gene-level between patients with and without autoimmunizations. Our finding suggest that gene signature of Treg cells isolated from SIgAD and CVID patients differ from age-matched healthy controls and form each other, while the occurrence of autoimmunity in both PID is associated with IFN signaling pathway. In sum, our findings improve our understanding of Treg dysfunctions in patients with common PIDs and associated autoimmunity.

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