The field of food allergy has seen tremendous change over the past 5-10 years with seminal studies redefining our approach to prevention and management and novel testing modalities in the horizon. Early introduction of allergenic foods is now recommended, challenging the previous paradigm of restrictive avoidance. The management of food allergy has shifted from a passive avoidance approach to active interventions that aim to provide protection from accidental exposures, decrease allergic reaction severity and improve the quality of life of food-allergic patients and their families. Additionally, novel diagnostic tools are making their way into the clinical practice with the goal to reduce the need for food challenges and assist physicians in the -- often complex -- diagnostic process. With all the new developments and available choices for diagnosis, prevention and therapy, shared decision-making has become a key part of the medical consultation, enabling patients to make the right choice for them, based on their values and preferences. Communication with patients has also become more complex over time, as patients are seeking advice online and through social media, but the information found online may be outdated, incorrect, or lacking in context. The role of the allergist has evolved to embrace all the above exciting developments and provide patients with the optimal care that fits their needs. In this review, we discuss recent developments, as well as the evolution of the field of food allergy in the next decade.

Predicting reaction threshold and severity are important to improve the management of food allergy, however the determinants of, and relationship between, these parameters are significant knowledge gaps. Identifying robust predictors could enable the reliable risk-stratification of food-allergic individuals. In this series of young people with CM-allergy undergoing DBPCFC – the largest reported in the literature – we did identify any baseline marker which predicted the occurrence of anaphylaxis at challenge, consistent with existing data. 1 There is one report of IgE-sensitisation being predictive of severity in CM-allergy, 5 however the authors included non-reactive patients in their analysis which significantly skewed the analyses, resulting in misleading conclusions. 6 IgE-sensitisation in our cohort, particularly to casein, was predictive of LOAEL. Including an assessment of casein IgE may therefore be of clinical utility when evaluating patients with CM-allergy in the clinical setting.

LETTER TO THE EDITORNo apparent impact of incremental dosing on eliciting dose at double-blind, placebo-controlled peanut challengeOlaya Álvarez García,1,2 Joan Bartra,1,3 Monica Ruiz-Garcia,1Isabel J. Skypala,1,4 Stephen R. Durham,1,4 Robert J. Boyle,1 E.N. Clare Mills,5 Paul J. Turner1

Food allergy is an increasingly common disease worldwide, and is thought to be driven by an uncontrolled type 2 immune response. Current knowledge about the underlying mechanisms that initiate and promote an inappropriate immune response to dietary allergens is limited. Sensitization through the skin in early life is considered to be a key event. Food allergy results from a dysregulated type 2 response to food allergens, characterized by enhanced levels of IgE, IL-4, IL-5 and IL-13 with infiltration of mast cells, eosinophils and basophils during acute reactions. Recent data implies a possible role of innate lymphoid cells (ILCs) in driving food allergy. ILCs represent a group of lymphocytes that lack specific, recombined antigen receptors. They contribute to immune responses not only through the release of cytokines and other mediators, but also by responding to cytokines produced by activated cells in their local microenvironment. Due to their localization at barrier surfaces of the airways, gut and skin, ILCs form a link between the innate and adaptive immunity. This review summarizes recent evidences on how skin and gastrointestinal mucosal immune system contribute to both homeostasis and the development of food allergy, as well as the involvement of ILCs towards inflammatory processes and regulatory mechanisms.

Background: There is increasing interest in the use of eliciting doses (EDs) to inform allergen risk management. EDs can be estimated from the distribution of threshold doses for allergic subjects undergoing food challenges within a specified population. Estimated ED05 values for cow’s milk (the dose expected to cause objective allergic symptoms in 5% of the milk-allergic population) range from 0.5mg to 13.9mg cow’s milk protein. We undertook a single-dose challenge study to validate a predicted ED05 for cow’s milk of 0.5mg protein. Methods: Participants were recruited from 4 clinical centres. Predetermined criteria were used to identify patients reacting to 0.5mg cow’s milk protein (approximately 0.015ml of fresh cow’s milk). Children over 1 year underwent formal challenge to cow’s milk to confirm clinical reactivity. Results: 172 children (median age 6 (IQR 0.7-11) years, 57% male) were included in this analysis. Twelve (7.0%, 95% CI 3.7-11.9%) children experienced objective symptoms that met the predetermined criteria. One participant had mild anaphylaxis which responded to a single dose of adrenaline, the remainder experienced only mild symptoms with no treatment required. We did not identify any baseline predictors of sensitisation which were associated with objective reactivity to the single-dose challenge using 0.5mg cow’s milk protein. Conclusions: These data support an estimated ED05 for cow’s milk of 0.5mg protein. Values for ED05 above 0.5mg for cow’s milk protein proposed for allergen risk management need to be reviewed.