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Future of food allergy

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Read time: 50 mins
Last updated:3rd Aug 2021
Published:3rd Aug 2021

Find out what the future holds for the diagnosis and treatment of food allergy by exploring:

  • The unmet needs of food allergy in our expert interview with Dr Alexandra Santos
  • Treatments currently being investigated or making their way to clinical practice in our infographic
  • Novel developments in diagnostic testing, such as the basophil and mast cell activation tests
In this section

Unmet needs in food allergy

Improving care is a multifaceted challenge, involving the development of new preventative measures and treatment as well as fostering proactive partnerships with patients to increase their educational awareness of the risks associated with food allergies1.

Instead of fear-based decisions, informed patients will then have the tools necessary to make evidence-based decisions and will be better able to manage the risks they face each day1.

Join Dr Alexandra Santos below where she describes the four key current unmet needs faced by patients with food allergy.

What are the unmet needs in the prevention of food allergy?

In 2015, the seminal Learning Early About Peanut Allergy (LEAP) study showed that the early introduction of peanut to infants had a significant positive effect in the prevention of peanut allergy2,3.

A key unmet need in the prevention of food allergy is the need to enhance and optimise the implementation of early food introduction to prevent the development food allergy1

Following the results of the LEAP study, and others, the European Academy of Allergy and Clinical Immunology (EAACI) and American Academy of Allergy, Asthma & Immunology (AAAAI) were updated in 2020 to add recommendations for the introduction of egg and peanut between the ages of four and six months4,5. However, challenges still remain.

A systematic review of twenty-eight food allergy prevention guidelines (1999–2019) was conducted to comprehensively appraise their quality for health professional use6.

Twenty-five guidelines were found to make recommendations on exclusive breastfeeding, AAACI, EAACI, Asia pacific association of paediatric allergy, Respirology & immunology (APAPARI), and Australasian Society of Clinical Immunology and Allergy (ASCIA). However, several guidelines made no exclusive feeding recommendations, such as the National Institute of Allergy and Infectious Diseases (NIAID) guidelines6.

Of the guidelines that did make recommendations, six recommended "exclusive/predominantly exclusive breastfeeding for at least 4 months” and seven recommended "exclusive breastfeeding for 6 months or around 6 months or at least 6 months"6.

While guideline recommendations vary, all recommend the early introduction of food within a 4–6 month range6

Twenty-seven guidelines make recommendations regarding the timing of solid food introduction into the infant diet. While these recommendations had a high variability, all were within a 4–6 month range. Specifically, sixteen guidelines recommend that common food allergen introduction should not be delayed6.

Notably, six documents were updated following the publication of the LEAP study to include peanut allergy specific information6.

Some guidelines also stratify patients based on risk, such as NIAID and American Academy of Pediatrics guidelines. Conversely, several guidelines have a universal introduction of early allergens6. A qualitative analysis of the EAT study (N=1,303) also revealed three main challenges to the early introduction of allergenic food3:

  • Refusal of some children to consume allergenic food
  • Caregiver concern over the potential for a reaction
  • Practical problems associated with the regimen compromising caregiver capacity to persist

There is also still little evidence available concerning the optimal dose and timing of allergenic foods for the prevention of food allergy7.

What are the unmet needs in the diagnosis of food allergy?

As the prevalence of food allergy increases, it is becoming ever more important to have accurate newer diagnostic tools that provide objective evidence and prevent the misdiagnosis of food allergy8.

Currently, the oral food challenge is the gold standard for identifying the threshold of responsiveness as well as diagnosis and monitoring food allergy. However, the procedure is burdensome, requiring a team of specialised health professionals to ensure the safety of the patient during the challenge9.

Misdiagnosis of food allergy and the missed recognition of severe reaction risk remains a challenge in the diagnosis of food allergy9

A previous meta-analysis (N=51) highlighted that self-reported food allergy prevalence was much higher than the prevalence estimates based on objective assessments, such as skin prick test (SPT), serum IgE (sIgE), or food challenge10. It was found that as many as 35% of people may report a food allergy, while only 1.0% to 10.8% have objective evidence confirmed with standardised testing10.

Inaccurate diagnosis through self-reporting may lead to potentially harmful malnutrition. In a UK study that investigated the growth status of food allergic children receiving dietetic input at 13 different centres (N=97), it was found that the elimination of ≥3 foods significantly impacted weight at various ages (P=0.044)11.

What are the unmet needs in the treatment of food allergy?

A key intervention in the management of food anaphylaxis is the complete avoidance of the food allergen12. This can however be a difficult goal to accomplish, as half of children who have a food allergy reaction have a second accidental exposure within two years9.

The undertreatment of accidental peanut exposure is also a well-established problem, with the use of adrenaline autoinjectors, following exposure, estimated to be as low as 1.1% per year13.

Research has shown that one of the highest-ranked unmet needs is the development of new treatments to reduce the severity of food allergies14

In a survey of parents from food allergy patient advocacy organisations, patients identified three main goals of treatment15:

  • 56% identified complete freedom to consume foods
  • 28% identified protection from accidental ingestion
  • 16% the ability to consume limited amounts with caution

However, a later qualitative study found that parents were willing to trade reduced efficacy gains for lower risks of therapy16.

As multiple therapies currently exist in clinical trials, the future holds the possibility of more robust treatment choices for single or multiple food allergies that are lasting, safe, and can prevent the development of allergic reactions following an accidental exposure1.

What are the unmet needs in the psychosocial impact of food allergy?

The mainstay of food allergy management is constant vigilance to avoid accidental exposure to allergens12,17. This burden, along with the unpredictable nature of allergic reactions, has been shown through research over the past twenty years to have an impact on quality of life18,19.

Anxiety, depression, and a decreased quality of life are associated with food allergies, however mental health issues may be under-recognised20

However, while research has increased into the psychiatric co-morbidities associated with food allergies, this needs to be incorporated more into clinical practice20.

There is also a scarcity of research on the prevalence rates of depression, anxiety, and post-traumatic stress disorder (PTSD) in patients with food allergies, and their caregivers. This likely means that mental health issues among people with food allergies are underreported and that healthcare professionals need to address these psychological and psychosocial needs20.

Emerging diagnostics for food allergy

While the clinical history remains the most valuable tool to reach an accurate diagnosis, several new objective biomarkers are currently being investigated, or are beginning to make their way into clinical practice21.

See Dr Alexandra Santos below for a brief overview of the diagnostic tests that are currently making their way into clinical trials.

Can IgE to individual allergen molecules be detected?

A recent advance in diagnostic testing for food allergy is component-resolved diagnosis (CRD), a diagnostic test utilising specific IgE to single allergens or components21.

CRD enables the identification of specific IgE against both major and minor allergens. Panallergens are allergens present in different sources and can cause IgE cross-reactivity. Examples include profilins, procalcins, non-specific lipid transfer proteins, and Bet v 1 homologues21. This increased capacity of CRD to identify and characterise specific molecules allows for a greater ability to21,22:

  • Predict the evolution of the allergic process
  • Differentiate species-specific and cross-reactive allergens
  • Determine the risk of a severe reaction
  • Guide and stratify the outcome of the OFC
  • Discriminate against primary food allergies and secondary sensitisation

In clinical practice, this allows CRD to help improve the accuracy of diagnostic testing, although the oral food challenge still remains the gold standard due to its greater specificity and sensitivity22.

Are basophil activation tests being used in clinical practice?

A novel test that is progressively transitioning into clinical practice is the basophil activation test (BAT)23. Processed within hours, flow cytometry is used to scan the surface of allergen-stimulated basophils to detect the expression of activation markers, such as CD63 and CD203c, following exposure to allergens24.

Functioning like an in vitro OFC, food extracts that are suspected of causing the allergic reaction are exposed to basophils to assess whether they degranulate upon stimulation24

BAT has been assessed for a variety of different food allergies and has reported sensitivity ranges from 77–98% and specificity from 75–100%, displaying a higher accuracy than SPT and sIgE23,24–33. In a more recent study that assessed the performance of BAT as a diagnostic marker for peanut allergy (N=104), BAT was shown to be superior to other diagnostic tests in differentiating peanut allergy and tolerance, have 100% specificity, and reduce the need for OFCs34. BATs have also been shown to correlate with severity of reaction at food challenge35.

What research is being carried out for mast cell activation tests?

While BAT has a high sensitivity and specificity when diagnosing food allergy, the test does have limitations. Notably, BAT requires whole fresh blood within 24–48 hours of sampling and has a 10–15% failure rate in the results due to non-responding basophils36.

These limitations have led to increased interest in the mast cell activation test (MAT), which benefits from using patient plasma to sensitise mast cells before allergen stimulation and analysis with flow cytometry36. MAT has been shown to have comparable specificity to BAT (98%), although with a lower sensitivity (73%)36.

However, both BAT and MAT have yet to progress fully into a clinical context or receive appropriate standardisation, validation, and quality assurance. Although these diagnostic tests may prove useful in the future for reducing the risk of allergic reactions during OFC and deciding when to use OFC24,34,37.

Investigational treatments for food allergy

The last decade of research has led to advances in the understanding of the pathophysiology of food allergy. Novel immunotherapies, biologic treatments, and therapies in the early stages of clinical trials offer the potential for increased safety, administration, and lasting tolerance38.

Join Dr Sharon Chinthrajah below, to discover the exciting developments in food allergy treatment that are currently under investigation39.

What allergen-specific approaches are being investigated?

In addition to the approval of peanut allergen powder for the treatment of peanut allergy for patients aged 4–17 years, various other oral immunotherapies (OITs) are currently being investigated (Figure 1, Table 1)38.

T4 Food Allergy_Fig1.png

Figure 1. Mechanisms of food allergy and investigational immunotherapy treatments (Adapted40). EPIT, epicutaneous immunotherapy; H1/2, histamine; IgE, immunoglobulin E; IgG, immunoglobulin G; IL, interleukin; ILC2, type 2 innate lymphoid cells; IT, immunotherapy; OIT, oral immunotherapy; PAMPs, pathogen-associated molecular patterns; SLIT, sublingual immunotherapy; TH2, T helper 2 cell; Treg, regulatory T cells; TSLP, thymic stromal lymphopoietin.

Other routes of exposure are also currently being investigated, including under the tongue with sublingual immunotherapies (SLITs) and through the skin with epicutaneous immunotherapies (EPITs), individually and in combination38.

OIT, SLIT, and EPIT are allergen-specific approaches utilising the progressive increase of exposure to a specific food allergen with the goal of reaching a daily maintenance dose to achieve desensitisation41,42.

Repeated exposure to the antigen through immunotherapy is believed to induce or restore tolerance to the allergen through decreased activation of mast cells and basophils due to decreased circulating immunoglobulin E (IgE), increased allergen-specific immunoglobulin G4 (IgG4)antibodies, and decreased T helper type 2 (TH2) cells43.

A comprehensive systematic review and meta-analysis (N=1,259), the efficacy and safety of OIT, SLIT, and EPIT management in food allergy were assessed44. In the twenty-seven trials included, they revealed a substantial benefit of OIT and SLIT compared to controls with respect to desensitisation (risk ratio [RR]=0.16, 95% CI 0.10, 0.26; Test for overall effect: Z=−7.582 [P<0.0001]). Eight studies also suggested a benefit to sustained unresponsiveness; however, this was not confirmed (RR=0.29, 95% CI 0.08, 1.13; Test for overall effect: Z=−1.788 [P<0.074])44.

Table 1 contains a non-exhaustive selection of published clinical studies in peanut allergy. In addition to these studies, other food allergens and methods of immunotherapy are actively being studied, including multi-allergen oral immunotherapy studies38.

Table 1. Overview of 2015 – 2021 published clinical studies, with DBPCFC inclusion criteria (Adapted45–47). DBPC, double blind placebo controlled; DBPCFC, double blind placebo controlled food challenge; EPIT, epicutaneous immunotherapy; M, months; OFC, oral food challenge; OIT, oral immunotherapy; PbO, placebo; pOIT, peanut oral immunotherapy; PP, peanut protein; ppOIT, peanut OIT plus probiotics; RCT, randomised controlled trial; SLIT sublingual immunotherapy; W, weeks.

*Safety data: only three subjects dropped out due to anaphylactic reactions (1.3%), and systemic allergic reactions occurred in eight patients (3.4%). †No DBPCFC inclusion criteria.
Group and cohort Clinical study design Efficacy and tolerability data
Oral Immunotherapy
2015: Tang et al. (PPOIT)
N=62
Age=1–10		 DBPC/RCT
Probiotics + pOIT vs PbO
18 M, 2000 mg		 ppOIT: 82.1% tolerated ≥4 g PP (2–5 W after therapy)
PbO: 3.6% tolerated ≥4 g PP (2–5 W after therapy)
2018: Bird et al. (ARC001)
N=55
Age=4–21		 Phase 2, multicentre, DBPC/RCT
AR101 vs PbO
20–36 W, 300 mg
 AR101: 79% tolerated ≥443 mg PP and 62% tolerated ≥1043 mg PP
PbO: 19% tolerated ≥443 mg PP and 0% tolerated ≥1043 mg PP
2018: Vickery, PALISADE Group (PALISADE) 
N=551
Age=4–55		 Phase 3, multicentre, DBPC/RCT
AR101 vs PbO
12 M, 300 mg
 AR101 (4–17): 76.6% tolerated 300 mg, 67.2% tolerated 600 mg, 50.3% tolerated 1 g PP in a single dose
PbO (4–17): 8.1% tolerated 300 mg, 4% tolerated 600 mg, 2.4% tolerated 1 g PP in a single dose
No statistical significance
AR101 (18–55): 41.5% tolerated 600 mg PP in a single dose
PbO (18–55): 14.3% tolerated 600 mg PP in a single dose
2019: Blümchen et al.
N=62
Age=3–17		 Multicentre, DBPC/RCT
Low-dose pOIT vs PbO
13 M, 125 mg, 250 mg
 Low-dose pOIT: 74.2% tolerated ≥300 mg PP, 41.9% tolerated 4.5 g PP
PbO: 16.1% tolerated ≥300 mg PP, 3.2% tolerated 4.5 g PP
2019: Chinthrajah et al. (POISED)
N=120
Age=7–55		 Randomised, double-blind, placebo-controlled, phase 2 study
OIT vs PbO
24M 4000 mg		 Primary outcome met with 35% of Peanut-0 group and 4% of the PbO group passing 4000 mg challenge at 104 and 117 weeks.
Significant difference between the Peanut-0 and Peanut-300 groups observed:
13% of Peanut-0 vs 37% of Peanut-300 participants completed the 4000 mg DBPCFC 12 months after OIT discontinuation.
Epicutaneous immunotherapy
2015: Sampson et al. (VIPES)
N=221
Age=6–55		 Phase 2b, multicentre, DBPC RCT
EPIT vs PbO
12 M, 50 µg, 100 µg, 250 µg		 10-Fold increase in cumulative threshold dose or ≥1 g PP in 50% of the 250 µg treatment group
(vs 25% in PbO group)
2016: Sampson et al. (OLFUS-VIPES)
N=173
83% VIPES participants		 Open-label, follow-up study (VIPES)
EPIT
24 M, 250 µg		 Results of the interim analysis (treatment duration, 24 months):
10-fold increase in cumulative threshold dose or ≥1 g PP in 69.7% of participants.
10-Fold increase in the cumulative threshold dose or ≥1 g PP in 80% of participants in the 6‑ to 11-year age group
2017: Jones et al. (CoFAR 6)
N=74
Age=4–25		 Phase 2, multicentre, DBPC/RCT
EPIT vs PbO
52 W, 100 µg, 250 µg
 10-Fold increase in cumulative threshold dose in 46% with 100 µg treatment, 48% with 250 µg treatment, 12% with PbO
2019: Fleischer et al. (PEPITES)*
N=356
Age=4–11		 Phase 3, multicentre, DBPC/RCT
EPIT vs PbO
12 M, 250 µg		 Increase in threshold dose (from <10 to ≥300 mg and from 10–300 mg to ≥1 g) in 35.3% with 250 µg treatment and 13.6% with PbO
2020: Fleischer et al. (PEOPLE)†
N=198
Age=4–11		 Open-label, follow-up study (PEPITES)
EPIT
36M 250 µg		 12M: increase in the threshold dose to ≥1000 mg in 40.4%
36M: increase in threshold dose to ≥1000 mg in 51.8%
Increase in threshold dose in 75.9%. 13.5% tolerated 5444mg peanut protein in the DBPCFC.
2021: Pongracic et al. (REALISE)†
N=393
Age=4–11		 Phase 3 randomised controlled trial
EPIT vs PbO
6M 250 µg		 Study complete, results not yet published.
Sublingual immunotherapy
2015: Narisety et al.
N=21
Age=7–13		 Monocentric, DBPC/RCT
SLIT vs OIT (active SLIT/ PbO OIT vs PbO SLIT/active OIT)
12 M, 3.7 mg (SLIT),
2000 mg (OIT)		 141-Fold increase in threshold dose (OIT group) vs 22-fold increase in threshold dose (SLIT group)
2021: Kim et al†
N=18
Age=1–11		 Monocentric, DBPC/RCT
SLIT vs PbO
12M 2000 µg
 Median cumulative tolerated dose: SLIT = 1710 mg peanut protein. PbO = 85 mg.

EPIT relies on the passive transfer of allergens via an adhesive dermal patch containing food protein to induce desensitisation38. A phase 2 multicentre, double-blind, randomised, placebo-controlled study (N=74) assessed the clinical, safety, and immunologic effects of peanut allergy48. The study demonstrated that EPIT was safe and associated with a modest treatment response after 52 weeks. Specifically, treatment success was achieved in 12% of the placebo-treated participants, 46% of the 100μg patch participants (P=0.005), and 48% of the 250μg patch participants (P=0.003)48.

Can the allergic immune cascade be targeted?

Parallel to the research on EPIT, OIT, and SLIT, there has been increasing research on monoclonal antibody therapies, such as omalizumab, ligelizumab, dupilumab. These new treatments aim to target the biology of the allergic inflammation cascade, giving rise to possible allergen non-specific treatments38.

Omalizumab is a widely investigated anti-IgE treatment that has already gained approval for allergic asthma and chronic idiopathic urticaria38

In food studies, omalizumab has been a useful treatment for facilitating rapid desensitisation, in combination with OIT, by reducing adverse reactions38 and improving speed of desensitization to multiple foods simultaneously49–52.

In a randomised, double-blind, placebo-controlled, multi-centre trial (N=37), omalizumab as an adjunct to peanut OIT allowed for rapid up-dosing of peanut OIT in eight weeks53. Six weeks after stopping treatment, 79% of subjects randomised to omalizumab tolerated 2000 mg of peanut protein, compared to 12% receiving placebo (P<0.01)53.

A 2021 multi-centre, randomised controlled clinical trial aims to further explore omalizumab as a therapy for food allergy. The OUtMATCH study will investigate omalizumab as a monotherapy as well as an adjunct therapy to OIT for patients with peanut allergy in addition to at least two other food allergies54.

Early investigations of ligelizumab and dupilumab

The next-generation, higher affinity, anti-IgE ligelizumab has been proposed as a treatment of food allergies as it prevents passive systemic anaphylaxis in human FcϵRIα transgenic mice55. In previous investigations, it has demonstrated an increased suppression of free IgE compared with omalizumab56.

As a dual inhibitor of interleukin (IL)-4 and IL-13 signalling, cytokines that are important in TH2 allergic inflammation, dupilumab is also a biologic of interest57. It is currently in trials to assess its ability to improve desensitisation, both as an adjunct to OIT and as a monotherapy58–60.

Are there targets higher in the allergic cascade?

Further up in the allergic cascade are alarmins that are critical in the development and maintenance of food allergies. Investigations of anti-alarmin agents for the treatment of food allergy are planned or currently underway61,62.

Anti-IL-33

A notable pilot study was the phase 2a randomised, placebo-controlled study of etokimab, an anti–IL-33 biologic, as a monotherapy for peanut allergy (N=20)63.

Efficacy measurements (a passed OFC of 275 mg peanut protein) demonstrated a pass rate of 73% versus 0% at day 15 (P = 0.008) and 57% versus 0% at day 45 (no significance) for etokimab and placebo, respectively63.

IL-4, IL-5, IL-9, IL-13, and ST2 levels in CD4+ T cells were reduced in the etokimab group compared to the placebo group upon peanut-induced T cell activation at day 15 (P=0.036 for IL-13 and IL-9). Peanut-specific IgE was also reduced in etokimab group compared to placebo at day 15 (P=0.014)63.

The results of this study give rise to the potential for an allergen non-specific approach to treating food allergy63.

Anti-IL-4/IL-13

In mouse models, blockade of IL-4/IL-13 signalling was seen to inhibit IgE production in vitro and in vivo and prevent anaphylaxis in allergen-challenged mice. Moreover, treatment with anti-IL-4Ra skewed the cytokine response by enhanced IL-10 and suppressing TH2 cytokine production64.

Future targets

Further targets that are currently under investigation for modifying the immune response include65–67:

  • ARA LAMP DNA vaccine
  • Vaccine development based on nanoparticles
  • Treatments for modifying gut microbiota

As all atopic diseases share common features, there is also the potential that treatments that are found to be successful in other atopic diseases, may prove to be of value in the future treatment of food allergy68.

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