Genetic predisposition to peanut allergy

The development of food allergy, as a complex condition, is influenced by both genetics and environment, as well as genome-environment interactions, including epigenetics.

Food allergy is an adverse immune response to certain foods. Food allergens are diverse, the most common being cow's milk, egg, peanuts, tree nuts, soy, wheat, fish and shellfish. In the last twenty years the prevalence of food allergy has increased markedly and now affects 8% of children and 11% of the adult population.

Peanut allergy is one of the most common food allergies in children, affecting 3% in the USA and 9.5% in Australia. Common food allergens in Asia are different from those observed in Western countries and it is suggested that the contribution of the environment to the development of food allergy is relevant.

Peanut allergy can appear during childhood and persist into adulthood, in the same way as nut allergy, seed allergy, fish allergy and shellfish allergy. Symptoms of peanut allergy usually develop within minutes to about two hours after ingestion of peanuts. Symptoms of peanut allergy can be highly variable (mild to severe) and include: itchy mouth, hives, redness, nausea and vomiting.

A family history of food allergy is considered one of the main risk factors, which is increased by 2 to 10 times. This suggests that in addition to environmental factors, genetics may play an important role in the development of food allergy.

Several recent studies, including a genome-wide association study involving individuals of European ancestry, have identified two variants associated with an increased risk of developing peanut allergy. These markers are significantly associated with DNA methylation, a process involved in gene expression.

DNA methylation is an epigenetic process involved in the downregulation of gene expression and can lead to gene silencing, i.e. genes are no longer expressed. Both variants are located in the HLA and FLG genes, both of which are the most studied genes in relation to food allergy.

The HLA gene encodes for the production of the major histocompatibility complex in humans, whose main function is to present antigenic peptides to T lymphocytes, responsible for the specific immune response to eliminate the pathogen. On the other hand, the FLG gene is responsible for producing filaggrin, a protein involved in the development and maintenance of the skin barrier. Variants in FLG have also been associated with skin disorders.

It should be noted that two genetic markers that have been related in the scientific literature to an increased individual susceptibility to develop peanut allergy are evaluated here, but as indicated above, there are other factors involved in the mechanisms of food allergy that can modulate its development, so this result should not be considered for diagnosis.

In clinical practice, IgE tests (skin prick test, SPT; serum specific IgE/sIgE), measurements of other serological parameters (e.g., serum IgE/sIgE), measurements of other serologicalserological parameters (e.g. total IgE, food-specific IgG4, sIgE/IgG4) and controlled oral administration of the suspected allergen.

Number of observed variants

13.5 million variants

Number of variants analyzed in the study

2 variants


Asai Y., Eslami A., et al. Genome-wide association study and meta-analysis in multiple populations identifies new loci for peanut allergy and establishes C11orf30/EMSY as a genetic risk factor for food allergy. J Allergy Clin Immunol. 2018 Mar;141(3):991-1001.

Czolk R., Klueber J., et al. IgE-Mediated Peanut Allergy: Current and Novel Predictive Biomarkers for Clinical Phenotypes Using Multi-Omics Approaches. Front Immunol. 2021 Jan 28;11:594350.

Hong X., Hao K., et al. Genome-wide association study identifies peanut allergy-specific loci and evidence of epigenetic mediation in US children. Nat Commun. 2015 Feb 24;6:6304.

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