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Interferon Signature in the Blood in Inflammatory Common Variable Immune Deficiency [Training 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: GSE51405 | GEO | 2014/01/09

SECONDARY ACCESSION(S): PRJNA222981

REPOSITORIES: GEO

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

2014-01-09 | GSE51404 | GEO

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

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2014-01-09 | E-GEOD-51405 | biostudies-arrayexpress

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

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Gastrointestinal symptoms and pathology in patients with Common variable immunodeficiency

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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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