Genome-wide meta-analysis implicates variation affecting mast cell biology in urticaria.

Urticaria genome-wide association study mast cells meta-analysis

Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
09 Sep 2023
Historique:
received: 29 04 2023
revised: 13 08 2023
accepted: 31 08 2023
pubmed: 11 9 2023
medline: 11 9 2023
entrez: 10 9 2023
Statut: aheadofprint

Résumé

Urticaria is characterized by inappropriate mast cell degranulation leading to the development of wheals and/or angioedema. Twin and family studies indicate that there is a substantial heritable component to urticaria risk. Our aim was to identify genomic loci at which common genetic variation influences urticaria susceptibility. Genome-wide association studies of urticaria (including all subtypes) from 3 European cohorts (UK Biobank, FinnGen, and the Trøndelag Health Study [HUNT]) were combined through statistical meta-analysis (14,306 urticaria cases and 650,664 controls). Cases were identified via electronic health care records from primary and/or secondary care. To identify putative causal variants and genes, statistical fine-mapping, colocalization, and interrogation of publicly available single-cell transcriptome sequencing resources were performed. Genome-wide significant associations (P < 5 × 10 Common genetic variation influencing the risk of developing urticaria was identified at 6 genomic loci. The relationship between genes with roles in mast cell biology and several association signals implicates genetic variability of specific components of mast cell function in the development of urticaria.

Sections du résumé

BACKGROUND BACKGROUND
Urticaria is characterized by inappropriate mast cell degranulation leading to the development of wheals and/or angioedema. Twin and family studies indicate that there is a substantial heritable component to urticaria risk.
OBJECTIVE OBJECTIVE
Our aim was to identify genomic loci at which common genetic variation influences urticaria susceptibility.
METHODS METHODS
Genome-wide association studies of urticaria (including all subtypes) from 3 European cohorts (UK Biobank, FinnGen, and the Trøndelag Health Study [HUNT]) were combined through statistical meta-analysis (14,306 urticaria cases and 650,664 controls). Cases were identified via electronic health care records from primary and/or secondary care. To identify putative causal variants and genes, statistical fine-mapping, colocalization, and interrogation of publicly available single-cell transcriptome sequencing resources were performed.
RESULTS RESULTS
Genome-wide significant associations (P < 5 × 10
CONCLUSION CONCLUSIONS
Common genetic variation influencing the risk of developing urticaria was identified at 6 genomic loci. The relationship between genes with roles in mast cell biology and several association signals implicates genetic variability of specific components of mast cell function in the development of urticaria.

Identifiants

pubmed: 37690594
pii: S0091-6749(23)01117-X
doi: 10.1016/j.jaci.2023.08.033
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Sheila Mary McSweeney (SM)

St. John's Institute of Dermatology, London, United Kingdom. Electronic address: sheila.mcsweeney@kcl.ac.uk.

Jake Saklatvala (J)

Department of Medical and Molecular Genetics, King's College London, London, United Kingdom.

Rossella Rispoli (R)

Department of Medical and Molecular Genetics, King's College London, London, United Kingdom.

Clarisse Ganier (C)

Center of Gene Therapy and Regenerative Medicine, King's College London, London, United Kingdom.

Grzegorz Woszczek (G)

School of Immunology and Microbial Sciences, King's College London, London, United Kingdom.

Laurent Thomas (L)

K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway; BioCore - Bioinformatics Core Facility, Norwegian University of Science and Technology, Trondheim, Norway.

Kristian Hveem (K)

K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway; HUNT Research Centre, Department of Public Health and Nursing, Norwegian University of Science and Technology, Levanger, Norway; Levanger Hospital, Nord-Trøndelag Hospital Trust, Trondheim University Hospital, Trondheim, Norway.

Mari Løset (M)

K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway; Department of Dermatology, Clinic of Orthopedics, Rheumatology and Dermatology, St. Olav's Hospital, Trondheim University Hospital, Trondheim, Norway.

Nick Dand (N)

Department of Medical and Molecular Genetics, King's College London, London, United Kingdom.

Christos Tziotzios (C)

St. John's Institute of Dermatology, London, United Kingdom.

Michael Simpson (M)

Department of Medical and Molecular Genetics, King's College London, London, United Kingdom.

John Alexander McGrath (JA)

St. John's Institute of Dermatology, London, United Kingdom.

Classifications MeSH