Abnormal SCID Newborn Screening and Spontaneous Recovery Associated with a Novel Haploinsufficiency IKZF1 Mutation

Springer Science and Business Media LLC - Tập 41 - Trang 1241-1249 - 2021
Hye Sun Kuehn1, Nicholas J. Gloude2,3, David Dimmock4, Mari Tokita4, Meredith Wright4, Sergio D. Rosenzweig1, Cathleen Collins5,6
1Immunology Service, Department of Laboratory Medicine, NIH Clinical Center, National Institutes of Health, Bethesda, USA
2Division of Hematology Oncology, Department of Pediatrics, University of California San Diego, San Diego, USA
3Rady Children’s Hospital San Diego, San Diego, USA
4Rady Children’s Institute for Genomic Medicine, San Diego, USA
5Rady Children's Hospital-San Diego, San Diego, USA
6Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, University of California San Diego, San Diego, USA

Tóm tắt

IKAROS, encoded by IKZF1, is a member of the IKAROS family of zinc-finger transcription factors playing critical roles in lymphocyte development, differentiation, and tumor suppression. Several studies demonstrated that IKZF1 mutations affecting DNA binding or homo-/hetero-dimerization are mostly associated with common variable immunodeficiency, combined immunodeficiency, or hematologic manifestations. Herein we report a likely de novo, nonsense IKZF1 mutation (p.C182*) in a baby with low T cell receptor excision circles (TREC) identified by newborn screening testing for severe combined immunodeficiency. The patient also presented a profound B cell deficiency at birth. Genetic, functional, immunologic, and clinical outcome data associated with this patient and her mutation were evaluated. Mutant p.C182* was detected in the cytoplasm of the patient’s primary cells, in contrast to wild type (WT) IKAROS protein, only detected in the nucleus. Functional in vitro assessments revealed that p.C182* was less stable than WT IKAROS protein and failed to bind to its target DNA binding sequence and dimerize with WT IKAROS protein, resulting in impaired pericentromeric targeting and transcriptional repression by means of haploinsufficiency. During follow-up, while a spontaneous recovery of TREC and T cells was observed, B cells improved but not to sustained normal ranges. Patients with IKAROS-associated diseases can present with SCID-like TREC values through newborn screening testing. IKZF1 mutations should be added to the low TREC differential, although spontaneous recovery has to be considered.

Tài liệu tham khảo

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