Allergic rhinitis and asthma should be considered as organ-specific inflammatory diseases in which the genetic background has determined a local overproduction of Th2-type cytokines and an over-expansion of particular APCs and T cells. Among the latter, a potential pathogenetic role could be assumed for natural killer T cells, expressing both invariant (Valpha24/Vbeta11) and classic alphabeta or gammadelta T-cell receptors. Recent studies support this notion and also suggest that surface pollen substances of nonprotein structure, such as lipid components recognized by CD1, could be viewed as one of the foreign materials against which the immune system of the allergic subject can mount a local inflammatory response.