| Literature DB >> 33436162 |
Kanika Kanchan1, Selene Clay2, Haritz Irizar3, Supinda Bunyavanich4, Rasika A Mathias5.
Abstract
Food allergy (FA), a growing public health burden in the United States, and familial aggregation studies support strong roles for both genes and environment in FA risk. Deepening our understanding of the molecular and cellular mechanisms driving FAs is paramount to improving its prevention, diagnosis, and clinical management. In this review, we document lessons learned from the genetics of FA that have aided our understanding of these mechanisms. Although current genetic association studies suffer from low power, heterogeneity in definition of FA, and difficulty in our ability to truly disentangle FA from food sensitization (FS) and general atopy genetics, they reveal a set of genetic loci, genes, and variants that continue to implicate the importance of barrier and immune function genes across the atopic march, and FA in particular. The largest reported effects on FA are from MALT1 (odds ratio, 10.99), FLG (average odds ratio, ∼2.9), and HLA (average odds ratio, ∼2.03). The biggest challenge in the field of FA genetics is to elucidate the specific mechanism of action on FA risk and pathogenesis for these loci, and integrative approaches including genetics/genomics with transcriptomics, proteomics, and metabolomics will be critical next steps to translating these genetic insights into practice.Entities:
Keywords: Dual Allergen hypothesis; FLG; Food allergy; HLA; atopic march; barrier genes; genetics; genomics; immune genes; peanut allergy
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Year: 2021 PMID: 33436162 PMCID: PMC8261836 DOI: 10.1016/j.jaci.2020.10.039
Source DB: PubMed Journal: J Allergy Clin Immunol ISSN: 0091-6749 Impact factor: 10.793