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Interferon Signature in the Blood in Inflammatory Common Variable Immune Deficiency [Test Set]

ABSTRACT: Transcriptional profiling was used to characterize the immunologic networks in subjects with CVID who have inflammatory complications to identify clues as to pathogenesis and potentially better modes of treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51404 | GEO | 2014/01/09

SECONDARY ACCESSION(S): PRJNA222980

REPOSITORIES: GEO

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Interferon Signature in the Blood in Inflammatory Common Variable Immune Deficiency [Training Set]

2014-01-09 | GSE51405 | GEO

Interferon Signature in the Blood in Inflammatory Common Variable Immune Deficiency [Test Set]

Project description:Transcriptional profiling was used to characterize the immunologic networks in subjects with CVID who have inflammatory complications to identify clues as to pathogenesis and potentially better modes of treatment. CVID subjects who fulfilled the standard diagnostic criteria, including significantly decreased levels of IgG, IgA, and/or IgM and poor or absent specific antibody production were enrolled. They were classified into, with or without characteristic inflammatory complications, as previously designated (hematologic or organ-specific autoimmunity, biopsy-proven granulomatous disease, or interstitial lung disease, lymphoid hyperplasia/ with splenomegaly or gastrointestinal inflammatory disease). 59 patients were included in the training set and 21 healthy controls and for test set 32 patients and 15 healthy controls. Disease controls included 6 X-linked agammaglobulinemia (XLA) patients and 15 healthy controls were included. Blood was taken before the interval intravenous immune globulin (Ig) infusions, or between subcutaneous administrations. The blood was collected using Tempus tubes and processed for microarray analysis.

2014-01-09 | E-GEOD-51404 | biostudies-arrayexpress

Interferon Signature in the Blood in Inflammatory Common Variable Immune Deficiency [Training Set]

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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=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.

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

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