A new approach to oral allergen immunotherapy for food allergy?

Abstract

Fauquert et al have re-looked at the approach for oral immunotherapy for peanut allergy to try and reduce the adverse effects without affecting efficacy.1, 2 They have used peanut in sealed capsules in what they call Gastro-Intestinal Delivery Oral Immunotherapy (GIDOIT) to bypass the upper gastrointestinal tract. They enrolled adolescents with a positive double-blind, placebo-controlled and oral peanut challenge. Using a randomised, double-blind and placebo-controlled trial design, gradually increasing doses (2-400 mg) of peanut or placebo in capsules were ingested daily over 24 weeks. A total of 17/21 participants in the peanut arm and 1/9 participants in the placebo arm tolerated 400 mg of peanut protein at follow-up (P < .001; Figure 1). Interestingly, oropharyngeal symptoms were similar in both arms although (mild) digestive adverse events were seen more often in the peanut arm (P = .02). There was 1 severe advent event (anaphylaxis required intramuscular adrenaline) in the peanut arm. So might this GIDOIT be a better approach to oral immunotherapy for food allergy? Or is the approach only reducing the local adverse effects without addressing the less frequent but more severe systemic ones? Only larger follow-on studies will answer this question. Also in this issue of the Journal, Hayen et al3 have looked at the allergenicity of the new 2S Ara h 7 isoforms compared to the Ara h 2 and 6 2S allergens. They utilised serum from 15 individuals with double-blind, placebo-controlled food challenge defined peanut allergy. Sensitisation to Ara h 7.0201 isoform was found to be most frequent (Figure 2). Ara h 7.0201 was as efficient as Ara h 2.0201 and 6.01 in inducing basophil degranulation. The authors speculate that Ara h 7.0201 might be helpful in improving our peanut allergy diagnostics given its unique epitopes and allergenicity. Finally, I would like to mention one of my co-editor's papers from last month's issue of the Journal of Allergy and Clinical Immunology. Wisniewski et al4 looked at the pathogenesis of severe asthma in childhood. They examined bronchoalveolar lavage (BAL) samples from 52 children with allergic and non-allergic, severe treatment-refractory asthma using flow cytometry and a multiplex assay. BAL was characterised by TH1 cells and related cytokines. Levels of TH17-associated mediators were also high. Type 2 innate lymphoid cells and basophils were rarely seen in BAL fluid, and IL-5, IL-33 and IL-28A/IFN-l2 were only increased in multi-sensitised children. This is rather a surprise as we consider severe childhood asthma to be a TH2 disease.5 The results ask questions about our approach to therapy in severe childhood asthma and make it questionable as to whether we can simple extrapolate from adult studies.