In the past 10 years we have witnessed exciting progress in understanding different facets of the complex biological phenomena that participate in an allergic reaction. However, most of the very basics questions that were formulated 20 or more years earlier are still valid, since no answer has been given to them. Characteristically, in 1978, in an article entitled,‘What makes an allergen an allergen’, Aas [1] wrote ‘why do some substances and some molecules act as allergens while others apparently do not?’This is a question of outmost importance since its elucidation will have an important impact on patient treatment and eventually on prophylaxis.

A domain in which great progress has been accomplished is that of T–cell biology. Indeed, we know a lot more about the mechanisms of T–cell activation and about T–helper cell subsets producing cytokines with opposing effects in the regulation of IgE. Today it is understood that the production of IgE is stimulated by cytokines IL–4 and IL–13 [2, 3] and inhibited by IFN–γ [4]. These cytokines are produced by distinct subsets of T–helper cells, the so–called Th2 and Th1, respectively [5]. The association between the IgE response against allergens and the deviation of the immune response (ir) to type 2 has been supported by studies showing that allergen–specific T–cell clones from allergic patients produce type–2 cytokines when stimulated in vitro [6, 7]. Therefore, we can reformulate the above question as follows: why does the immune response against some substances (allergens) deviate to a type–2 cytokine profile?