| Literature DB >> 31897776 |
Adrian M Shields1, Bradly M Bauman2, Chantal E Hargreaves3,4, Andrew J Pollard5, Andrew L Snow2, Smita Y Patel3,4.
Abstract
Germline gain-of-function mutations in CARD11 lead to the primary immunodeficiency, B cell expansion with NF-κB, and T cell anergy (BENTA). Herein, we report the case of a girl, presenting at 2 years of age with lymphocytosis and splenomegaly in whom a novel, in-frame, three base pair deletion in CARD11 was identified resulting in the deletion of a single lysine residue (K215del) from the coiled-coil domain. In vitro functional assays demonstrated that this variant leads to a subtle increase in baseline NF-κB signaling and impaired proliferative responses following T cell receptor and mitogenic stimulation. Previously reported immunological defects associated with BENTA appear mild in our patient who is now 6 years of age; a B cell lymphocytosis and susceptibility to upper respiratory tract infections persist; however, she has broad, sustained responses to protein-polysaccharide conjugate vaccines and displays normal proliferative responses to ex vivo T cell stimulation.Entities:
Keywords: BENTA; CARD11; Primary immunodeficiency
Mesh:
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Year: 2020 PMID: 31897776 DOI: 10.1007/s10875-019-00729-x
Source DB: PubMed Journal: J Clin Immunol ISSN: 0271-9142 Impact factor: 8.317