Nearly 20 years ago, Kjell Aas presented the allergy and imtnunology communities with the thought-provoking question'What makes an allergen?"[1]. An answer to this question and a rational mechanism to account for why certain individuals become sensitized to allergens are essential to the understanding of the immediate hypersensitivity response, as well as to the design of better diagnostic tests and more effective therapeutic approaches. In the intervening years there has been exciting progress in understanding the nature of the T-cell receptor, in characterizing the molecular attributes important in antigen recognition and in the genetics of atopy. However, several probletns remain unsolved, and a full answer to the scientific challenge laid down by Aas remains to be provided. The absence of complete structural information for several major allergens currently prevents a full analysis of their antigcnic determinants and the possibility that there is a defective regulation of IgE responses in certain individuals also requires further investigation. Moreover, there is neither a definitive explanation of how airborne allergens gain access to imtnunocomponent cells, nor is the identity of the cells involved firmly established. However, data from recent research into the structural and functional aspects of house dust mite allergens have suggested a unifying mechanism by which presentation may occur, although work will be necessary to refine and substantiate this provocative hypothesis in order to assess its importance relative to other factors.