Travelling with Anisakis allergens.

clature Subcommittee (http://www.allergen.org/). Two of these, Ani s 2 (paramyosin) and Ani s 3 (tropomyosin), are considered pan-allergens with low specificity [13] , which makes them unsuitable as specific targets for immunoassays. The remaining group includes 3 major allergens (Ani s 1, Ani s 7, and Ani s 12) and 7 minor allergens (Ani s 4, Ani s 5, Ani s 6, Ani s 8, Ani s 9, Ani s 10, and Ani s 11). In a recent issue of the International Archives of Allergy and Immunology, Caballero et al. [14] focused on the importance of using component-resolved diagnosis to reveal IgE sensitization to Anisakis to avoid problems related to specificity while maintaining good sensitivity. The study was carried out by comparison of the specific IgE responses in sera from symptomatic and asymptomatic patients in Italy and Spain against a panel of 4 recombinant Anisakis allergens (Ani s 1, Ani s 5, Ani s 9, and Ani s 10; response measured by dot blot assay) and a purified native allergen (Ani s 4; response measured by Western blot). The authors reported differences in IgE recognition patterns between the two populations under study, as well as a predominance of gastrointestinal over allergic symptoms in the Italian population. These observations underline the importance of using selected allergenic components for the accurate diagnosis of Anisakis induced IgE sensitization in different populations. Differences in IgE reactivity in sera from patients infected with Anisakis may reflect interindividual variations in immunological responses or a different frequency of exposure, as reported for other allergens [15] ; however, such differences may also be due to a bias in patient selection when comparing different populations. In the study by CabalThe ability of Anisakis L3 larvae to infect humans and provoke gastrointestinal disorders was first recognized more than 50 years ago. However, it was not until the early 1990s that infections by this genus of nematodes were found to cause allergic reactions ranging from urticaria to anaphylaxis [1, 2] . More recently, it has been reported that the immunological/inflammatory changes brought about by previous infections involving this parasite can potentiate NSAID-induced upper gastrointestinal bleeding [3] . Anisakis allergens are frequently classified as food allergens because they are present in sea fish [4] . However, Anisakisinduced allergy differs from food allergy because it does not require an atopic predisposition and because for presentation of clinical symptoms the Anisakis allergens must enter the tissues of the alimentary tract at certain locations (e.g. the submucosa of the stomach) [5] . The hypothesis that Anisakis only provokes allergic symptoms when it parasitizes the alimentary tract was confirmed in provocation studies showing that patients with allergy to Anisakis tolerate ingestion of Anisakis allergens [6–8] . However, the possibility that the induction of IgE antibodies also requires infection by the parasite was suggested by epidemiological studies showing that such antibodies only occur in populations at risk (i.e. those consuming raw or undercooked sea fish) [9] . Historically, laboratory-based diagnosis of Anisakis IgE sensitization has mainly been done with whole parasite extracts (e.g. ImmunoCap and Western blot) [10] , defined antigens recognized by monoclonal antibodies [11] , and, more recently, recombinant allergens [12] . To date, 12 Anisakis allergens (Ani s 1 to Ani s 12) have been officially recognized by the WHO/IUIS Allergen NomenPublished online: March 6, 2014