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Our results suggest that the immunological mechanisms underlying the sustained response after 2 years of cessation of immunotherapy (3-year treatment period) are linked to the acquisition and maintenance of a regulatory T-cell response.

Objective: To define the sensitization pattern of patients with anaphylaxis to Vespa velutina nigrithorax (VVN). Methods: One-hundred consecutive Spanish patients with Hymenoptera anaphylaxis were studied. We systematically determined specific IgE (sIgE) to whole venoms (Vespula spp., Polistes dominula, Apis mellífera, Vespa crabro, Dolichovespula maculata) and their molecular components (rApi m 1, rApi m 5, rApi m 10, rVes v 1, rVes v 5, rPol d 5, cross-reactive carbohydrates). Specific IgE to VVN venom and its antigen-5 (nVesp v 5) were measured in a subsample. Results: Seventy-seven patients had VVN anaphylaxis. Of these, only 16 (20.8%) reported previous VVN stings but were stung by other Hymenoptera. Positive (>0.35 kU A /L) sIgE to each of the whole venoms was detected in >70% of patients (Vespula spp. in 100%). Components showing >50% positivity were rApi m 5 (51.4%), rPol d 5 (80.0%), and rVes v 5 (98.7%). This pattern was similar to that of patients with Vespula spp. anaphylaxis (n=11) but different from that of Apis mellifera anaphylaxis (n=10). Specific IgE to nVesp v 5 was positive in all studied patients (n=15) with VVN anaphylaxis and was correlated with sIgE to both rVes v 5 (R=0.931) and rPol d 5 (R=0.887). Conclusions: VVN has become the commonest cause of Hymenoptera anaphylaxis in our area. Most cases report no previous VVN stings. Their sensitization pattern is similar to that of patients with anaphylaxis to other Vespidae. Specific IgE to antigen-5 from VVN, Vespula spp., and Polistes dominula are strongly correlated in patients with VVN anaphylaxis.

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Background: Anisakiasis is caused by the consumption of raw or undercooked fish or cephalopods parasitized by live L3 larvae of nematode Anisakis spp. Larvae anchor to stomach mucosa releasing excretion/secretion products which contain the main allergens. It has been described that nematode larvae release venom allergen-like proteins among their excretion/secretion products. We investigated potential cross-reactivity between Anisakis and wasp venom allergens. Methods: Two groups of 25 patients each were studied: wasp venom- and Anisakis-allergic patients. Sera from patients were tested by ImmunoCAP, dot-blotting with recombinant Anisakis allergens and ADVIA-Centaur system with Hymenoptera allergens. Cross-reactivity was assessed by IgE immunoblotting inhibition assays. Role of cross-reactive carbohydrate determinants (CCDs) was studied by inhibition with bromelain and periodate treatment. Results: A total of 40% of wasp venom-allergic patients had specific IgE to Anisakis simplex and 20% detected at least one of the Anisakis recombinant allergens tested. Likewise, 44% of Anisakis-allergic patients had specific IgE to Vespula spp. venom and 16% detected at least one of the Hymenoptera allergens tested. Wasp venom-allergic patients detected CCDs in Anisakis extract and peptide epitopes on Anisakis allergens rAni s 1 and rAni s 9, whereas Anisakis-allergic patients only detected CCDs on nVes v 1 allergen from Vespula spp. venom. The only Anisakis allergen inhibited by Vespula venom was rAni s 9. Conclusions: This is the first time that cross-sensitization between wasp venom and Anisakis is described. CCDs are involved in both cases; however, peptide epitopes are only recognized by wasp venom-allergic patients.