| Literature DB >> 26529633 |
Michaela Kuhlen1, Andrea Hönscheid1, Loizos Loizou2, Schafiq Nabhani1, Ute Fischer1, Polina Stepensky3, Jörg Schaper4, Wolfram Klapper5, Meinolf Siepermann1, Friedhelm Schuster1, Roland Meisel1, Arndt Borkhardt6.
Abstract
PIK3R1 (phosphoinositide-3-kinase, regulatory subunit 1) gain-of-function has recently been described in patients with recurrent sinopulmonary infections, chronic CMV-/EBV-infections, lymphoproliferation, and hypogammaglobulinemia. Here we report a 15-year-old boy with treatment refractory CMV lymphadenitis, severe combined immunodeficiency, microcephaly and a severe developmental defect of Th17 cells. To avoid poor outcome, hematopoietic stem cell transplantation (HSCT) was performed. Subsequently, whole exome sequencing revealed a de novo heterozygous G-to-C mutation (chr5: 5:67,589,663: G>C) at the splice donor site of the PIK3R1 gene. Our data suggest that PIK3R1 gain-of-function leads to developmental defects in helper and regulatory T-cell subsets, the latter expanding the immunological features of PIK3R1 gain-of-function. T-cell subsets play a critical role in the regulation of immune response against infectious agents and of autoimmunity and thus may be particularly accountable for the clinical phenotype of affected patients.Entities:
Keywords: Chronic CMV infection; Immunodeficiency; Lymphoproliferation; PIK3R1; TH17 cells
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Year: 2015 PMID: 26529633 DOI: 10.1016/j.clim.2015.10.008
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969