This observation could be explained by cross-reactivity between arthropod allergens and Toxocara antigens as described above [45], [46] by inducing production of allergen-specific IgE by plasma cells through polyclonal signals associated with helminth infections such as IL-4 or by the fact that children who develop strong Th2 responses to Toxocara may be more ‘atopic’ in the sense that they are more likely to develop IgE responses to environmental allergens. Here, IGHE is linked to helminthiasis.