A novel CARD11 heterozygous missense variant in a CADINS patient

Background: CARD11-associated atopy with dominant interference of NF-κB signaling (CADINS) is developed as a result of heterozygous loss-of-function variants in CARD11 that function as strong dominant-negative alleles. In lymphocytes, CARD11 encodes a scaffold protein that links activation of the an...

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Main Authors: Randa S. AlYafie, PhD, Mehdi Adeli, MD, Dinesh Velayutham, PhD, Salim Bougarn, PhD, Manar Ata, MSc, Fatima Al-Ali, MRes, Evonne Chin-Smith, PhD, Bradly M. Bauman, PhD, Andrew L. Snow, PhD, Bertrand Boisson, PhD, Nico Marr, PhD, Nicholas van Panhuys, PhD, Andrea Guennoun, PhD, Puthen Veettil Jithesh, PhD
Format: Article
Language:English
Published: Elsevier 2025-05-01
Series:Journal of Allergy and Clinical Immunology: Global
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Online Access:http://www.sciencedirect.com/science/article/pii/S2772829325000621
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author Randa S. AlYafie, PhD
Mehdi Adeli, MD
Dinesh Velayutham, PhD
Salim Bougarn, PhD
Manar Ata, MSc
Fatima Al-Ali, MRes
Evonne Chin-Smith, PhD
Bradly M. Bauman, PhD
Andrew L. Snow, PhD
Bertrand Boisson, PhD
Nico Marr, PhD
Nicholas van Panhuys, PhD
Andrea Guennoun, PhD
Puthen Veettil Jithesh, PhD
author_facet Randa S. AlYafie, PhD
Mehdi Adeli, MD
Dinesh Velayutham, PhD
Salim Bougarn, PhD
Manar Ata, MSc
Fatima Al-Ali, MRes
Evonne Chin-Smith, PhD
Bradly M. Bauman, PhD
Andrew L. Snow, PhD
Bertrand Boisson, PhD
Nico Marr, PhD
Nicholas van Panhuys, PhD
Andrea Guennoun, PhD
Puthen Veettil Jithesh, PhD
author_sort Randa S. AlYafie, PhD
collection DOAJ
description Background: CARD11-associated atopy with dominant interference of NF-κB signaling (CADINS) is developed as a result of heterozygous loss-of-function variants in CARD11 that function as strong dominant-negative alleles. In lymphocytes, CARD11 encodes a scaffold protein that links activation of the antigen receptor with downstream signaling. Patients with CADINS generally experience severe atopic dermatitis, asthma, recurrent pneumonia and other upper respiratory tract infections, skin infections, and allergies to a variety of dietary and environmental antigens. Additionally, patients experience elevated levels of serum IgE, but low to normal levels of other immunoglobulin types. Objective: We performed genetic diagnosis of a patient of nonconsanguineous descent presenting at 11 years of age with severe atopic dermatitis, asthma, food allergy, skin and recurrent infections, and an extremely elevated level of serum IgE. Methods: We performed whole genome sequencing of samples obtained from the patient and his entire family. Results: Clinical, laboratory, genetic, and functional findings suggested CADINS. Genetic evaluation revealed a novel heterozygous missense variant (c.2913C>G, p.Cys971Trp) in the CARD11 gene as the potential underlying defect. Expression of CARD11 variant–stimulated constitutive NF-κB activity in T-cell lines demonstrated both loss-of-function and dominant-negative activity. Conclusion: A novel germline heterozygous missense variant (c.2913C>G) in CARD11 potentially leads to CADINS.
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spelling doaj-art-2be1e1de63cb4cbda5b48da5c301e7012025-08-20T01:51:13ZengElsevierJournal of Allergy and Clinical Immunology: Global2772-82932025-05-014210046110.1016/j.jacig.2025.100461A novel CARD11 heterozygous missense variant in a CADINS patientRanda S. AlYafie, PhD0Mehdi Adeli, MD1Dinesh Velayutham, PhD2Salim Bougarn, PhD3Manar Ata, MSc4Fatima Al-Ali, MRes5Evonne Chin-Smith, PhD6Bradly M. Bauman, PhD7Andrew L. Snow, PhD8Bertrand Boisson, PhD9Nico Marr, PhD10Nicholas van Panhuys, PhD11Andrea Guennoun, PhD12Puthen Veettil Jithesh, PhD13College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar; Research Department, Sidra Medicine, Doha, QatarDepartment of Allergy and Immunology, Sidra Medicine, Doha, Qatar; Hamad Medical Corporation, Doha, QatarCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, QatarResearch Department, Sidra Medicine, Doha, QatarResearch Department, Sidra Medicine, Doha, QatarResearch Department, Sidra Medicine, Doha, QatarResearch Department, Sidra Medicine, Doha, QatarDepartment of Pharmacology & Molecular Therapeutics, Uniformed Services, University of the Health Sciences, Bethesda, MdDepartment of Pharmacology & Molecular Therapeutics, Uniformed Services, University of the Health Sciences, Bethesda, MdThe Rockefeller University, New York, NYCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar; Research Department, Sidra Medicine, Doha, Qatar; Corresponding authors: Andrea Guennoun, PhD, Nicholas van Panhuys, PhD, or Nico Marr, PhD, Research Department, Sidra Medicine, Doha, Qatar.College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar; Research Department, Sidra Medicine, Doha, Qatar; Corresponding authors: Andrea Guennoun, PhD, Nicholas van Panhuys, PhD, or Nico Marr, PhD, Research Department, Sidra Medicine, Doha, Qatar.Research Department, Sidra Medicine, Doha, Qatar; Corresponding authors: Andrea Guennoun, PhD, Nicholas van Panhuys, PhD, or Nico Marr, PhD, Research Department, Sidra Medicine, Doha, Qatar.College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar; Pharmacology and Therapeutics, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, United Kingdom; Puthen Veettil Jithesh, PhD, College of Health & Life Sciences, Hamad Bin Khalifa University, C-147, Penrose House, PO Box 34110, Education City, Doha, Qatar.Background: CARD11-associated atopy with dominant interference of NF-κB signaling (CADINS) is developed as a result of heterozygous loss-of-function variants in CARD11 that function as strong dominant-negative alleles. In lymphocytes, CARD11 encodes a scaffold protein that links activation of the antigen receptor with downstream signaling. Patients with CADINS generally experience severe atopic dermatitis, asthma, recurrent pneumonia and other upper respiratory tract infections, skin infections, and allergies to a variety of dietary and environmental antigens. Additionally, patients experience elevated levels of serum IgE, but low to normal levels of other immunoglobulin types. Objective: We performed genetic diagnosis of a patient of nonconsanguineous descent presenting at 11 years of age with severe atopic dermatitis, asthma, food allergy, skin and recurrent infections, and an extremely elevated level of serum IgE. Methods: We performed whole genome sequencing of samples obtained from the patient and his entire family. Results: Clinical, laboratory, genetic, and functional findings suggested CADINS. Genetic evaluation revealed a novel heterozygous missense variant (c.2913C>G, p.Cys971Trp) in the CARD11 gene as the potential underlying defect. Expression of CARD11 variant–stimulated constitutive NF-κB activity in T-cell lines demonstrated both loss-of-function and dominant-negative activity. Conclusion: A novel germline heterozygous missense variant (c.2913C>G) in CARD11 potentially leads to CADINS.http://www.sciencedirect.com/science/article/pii/S2772829325000621CARD11CADINSeczemaasthmafood allergiesloss-of-function variant
spellingShingle Randa S. AlYafie, PhD
Mehdi Adeli, MD
Dinesh Velayutham, PhD
Salim Bougarn, PhD
Manar Ata, MSc
Fatima Al-Ali, MRes
Evonne Chin-Smith, PhD
Bradly M. Bauman, PhD
Andrew L. Snow, PhD
Bertrand Boisson, PhD
Nico Marr, PhD
Nicholas van Panhuys, PhD
Andrea Guennoun, PhD
Puthen Veettil Jithesh, PhD
A novel CARD11 heterozygous missense variant in a CADINS patient
Journal of Allergy and Clinical Immunology: Global
CARD11
CADINS
eczema
asthma
food allergies
loss-of-function variant
title A novel CARD11 heterozygous missense variant in a CADINS patient
title_full A novel CARD11 heterozygous missense variant in a CADINS patient
title_fullStr A novel CARD11 heterozygous missense variant in a CADINS patient
title_full_unstemmed A novel CARD11 heterozygous missense variant in a CADINS patient
title_short A novel CARD11 heterozygous missense variant in a CADINS patient
title_sort novel card11 heterozygous missense variant in a cadins patient
topic CARD11
CADINS
eczema
asthma
food allergies
loss-of-function variant
url http://www.sciencedirect.com/science/article/pii/S2772829325000621
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