PIK3R1 Mutation Associated with Hyper IgM (APDS2 Syndrome): A Case Report and Review of the Literature.


Journal

Endocrine, metabolic & immune disorders drug targets
ISSN: 2212-3873
Titre abrégé: Endocr Metab Immune Disord Drug Targets
Pays: United Arab Emirates
ID NLM: 101269157

Informations de publication

Date de publication:
2019
Historique:
received: 12 11 2018
revised: 08 01 2019
accepted: 07 02 2019
pubmed: 26 2 2019
medline: 31 3 2020
entrez: 26 2 2019
Statut: ppublish

Résumé

APDS [Activated phosphoinositide 3-kinase (PI3K) δ Syndrome] is a newly found special form of primary immunodeficiency caused by mutations in genes encoding PI3Kδ subunits and over-activation of the PI3K signaling pathway. Gain-of-function and loss-of-function mutations in PIK3CD (encoding P110δ) and PIK3R1 (encoding p85α, p55α and p50α) lead to APDS1 and APDS2, respectively. The subsequent irregular PI3K downstream signaling cascade is associated with abnormalities in B cells and T cells and the consequent heterogeneous clinical manifestations including respiratory tract infections, autoimmunity, lymphoproliferation and not to mention primary antibody deficiency. In this study, we report a 12-year-old girl with a mutation in the PIK3R1 gene who manifested immunological phenotypes resembling hyper IgM syndrome along with a review of the literature of the previously reported patients. Whole exome sequencing was performed to detect the underlying genetic mutation in this patient. A de novo heterozygous splice site mutation in the hot spot of the PIK3R1 gene within the intron 10 was found (c.1425+1G>A). Further investigations are required for evaluation of the underlying genetic defects and the possible associations between genetic underpinning and heterogeneous severity and features of the disease.

Sections du résumé

BACKGROUND AND OBJECTIVE OBJECTIVE
APDS [Activated phosphoinositide 3-kinase (PI3K) δ Syndrome] is a newly found special form of primary immunodeficiency caused by mutations in genes encoding PI3Kδ subunits and over-activation of the PI3K signaling pathway. Gain-of-function and loss-of-function mutations in PIK3CD (encoding P110δ) and PIK3R1 (encoding p85α, p55α and p50α) lead to APDS1 and APDS2, respectively. The subsequent irregular PI3K downstream signaling cascade is associated with abnormalities in B cells and T cells and the consequent heterogeneous clinical manifestations including respiratory tract infections, autoimmunity, lymphoproliferation and not to mention primary antibody deficiency. In this study, we report a 12-year-old girl with a mutation in the PIK3R1 gene who manifested immunological phenotypes resembling hyper IgM syndrome along with a review of the literature of the previously reported patients.
METHODS METHODS
Whole exome sequencing was performed to detect the underlying genetic mutation in this patient.
RESULTS RESULTS
A de novo heterozygous splice site mutation in the hot spot of the PIK3R1 gene within the intron 10 was found (c.1425+1G>A).
CONCLUSION CONCLUSIONS
Further investigations are required for evaluation of the underlying genetic defects and the possible associations between genetic underpinning and heterogeneous severity and features of the disease.

Identifiants

pubmed: 30799802
pii: EMIDDT-EPUB-96842
doi: 10.2174/1871530319666190225114739
doi:

Substances chimiques

PIK3R1 protein, human EC 2.7.1.-
Class I Phosphatidylinositol 3-Kinases EC 2.7.1.137
Class Ia Phosphatidylinositol 3-Kinase EC 2.7.1.137

Types de publication

Case Reports Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

941-958

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Reza Yazdani (R)

Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran, and the University of Medical Science, Tehran, Iran.

Zahra Hamidi (Z)

Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

Fateme Babaha (F)

Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

Gholamreza Azizi (G)

Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran.

Saba Fekrvand (S)

Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran, and the University of Medical Science, Tehran, Iran.

Hassan Abolhassani (H)

Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran, and the University of Medical Science, Tehran, Iran.
Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.

Asghar Aghamohammadi (A)

Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran, and the University of Medical Science, Tehran, Iran.

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Classifications MeSH