| Literature DB >> 23319571 |
Elisabeth Salzer1, Elisangela Santos-Valente, Stefanie Klaver, Sol A Ban, Wolfgang Emminger, Nina Kathrin Prengemann, Wojciech Garncarz, Leonhard Müllauer, Renate Kain, Heidrun Boztug, Andreas Heitger, Klaus Arbeiter, Franz Eitelberger, Markus G Seidel, Wolfgang Holter, Arnold Pollak, Winfried F Pickl, Elisabeth Förster-Waldl, Kaan Boztug.
Abstract
Primary B-cell disorders comprise a heterogeneous group of inherited immunodeficiencies, often associated with autoimmunity causing significant morbidity. The underlying genetic etiology remains elusive in the majority of patients. In this study, we investigated a patient from a consanguineous family suffering from recurrent infections and severe lupuslike autoimmunity. Immunophenotyping revealed progressive decrease of CD19(+) B cells, a defective class switch indicated by low numbers of IgM- and IgG-memory B cells, as well as increased numbers of CD21(low) B cells. Combined homozygosity mapping and exome sequencing identified a biallelic splice-site mutation in protein C kinase δ (PRKCD), causing the absence of the corresponding protein product. Consequently, phosphorylation of myristoylated alanine-rich C kinase substrate was decreased, and mRNA levels of nuclear factor interleukin (IL)-6 and IL-6 were increased. Our study uncovers human PRKCD deficiency as a novel cause of common variable immunodeficiency-like B-cell deficiency with severe autoimmunity.Entities:
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Year: 2013 PMID: 23319571 PMCID: PMC3630826 DOI: 10.1182/blood-2012-10-460741
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113