The following is a summary of “Filaggrin loss-of-function mutations are associated with persistence of milk and egg allergy,” published in the November 2022 issue of Allergy and clinical immunology by Kalb, et al.

The root cause of eczema and related allergic airway illnesses is a genetic flaw in the epidermal barrier protein filaggrin (FLG). The extent to which FLG loss-of-function (LOF) mutations contribute to the emergence and maintenance of food allergies is still up for debate. For a study, researchers sought to examine the relationship between FLG LOF mutations and allergic responses to various foods as well as their possible impact on the persistence of childhood food allergies.

For the German Genetics of Food Allergy Study (GOFA), 890 kids with food allergies that may be challenged were enrolled in this study. 684 kids’ longitudinal data were accessible. All children underwent clinical evaluation, including testing for food allergies, and were genotyped for the four most prevalent LOF variants in FLG: R501X, 2282del4, R2447X, and S3247X. By utilizing the German Multicenter Allergy Study cohort as the control group, logistic regression was used to examine associations between FLG mutations and food allergies.

With comparable risk estimations, FLG mutations were linked to allergies to various foods, including hen’s egg (HE), cow’s milk (CM), peanut, hazelnut, fish, soy, cashew, walnut, and sesame. After accounting for the eczema state, the effects were still profound. Interestingly, FLG mutations enhanced the chance of HE and CM allergies developing over time.

The study showed that FLG LOF mutations gave a risk of any food allergy irrespective of eczema using the gold standard for food allergy diagnosis. The mutations should be taken into account when evaluating the development of tolerance since they predispose to the persistence of HE and CM allergy.