Th2 responses induced by allergens or helminths share many common features. However, allergen-specific IgE can almost always be detected in atopic patients, whereas helminth-specific IgE is often not detectable and anaphylaxis often occurs in atopy but not helminth infections. This may be due to T regulatory responses induced by the helminths or the lack of helminth-specific IgE. Alternatively non-specific IgE induced by the helminths may protect from mast cell or basophil degranulation by saturating IgE binding sites. Both of these mechanisms have been implicated to be involved in helminth-induced protection from allergic responses. An article in the current issue of the European Journal of Immunology describes the generation of an anti-Nippostrongylus brasiliensis-specific IgE antibody which was used to identify a novel N. brasiliensis antigen (Nb-Ag1). The authors demonstrated that Nb-Ag1 specific IgE could only be detected for a short period of time during infection, and that these levels were sufficient to prime mast cells thereby leading to active cutaneous anaphylaxis after the application of Nb-Ag1. This is the first report clearly showing that a low level of helminth-specific IgE, transiently produced, is able to induce mast cell degranulation in the presence of large amounts of polyclonal IgE.