Pathogenetic aspects of allergic respiratory syndromes

Over the past twenty years great research effort has been made to clarify the pathogenetic mechanisms of allergic rhinitis (AR) and bronchial asthma (BA). The discovery of two types of Fc epsilon receptors (Fc epsilon RI and Fc epsilon RII) has made it possible to understand that allergic reactions can be due to interactions between allergens and cytophilic IgE bound not only by mast cells and basophils, but also by macrophages, lymphocytes, eosinophils and platelets. Knowledge of the complex mechanisms which regulate IgE antibody production has substantially improved since it was shown that IL-4 and T/B cell interactions are essential for the induction of human IgE synthesis, whereas IFN-gamma plays a negative regulatory role. In mice and humans, two types of helper T cells (Th1 and Th2) have been recognized, they produce different cytokines resulting in both cross-regulation of T cell function and B cell activity. In view of their particular pattern of cytokine secretion, Th2-type cells would be important in the specific response to allergens and in allergic inflammation. New knowledge about the mechanisms involved in the effector phase of allergic reactions and respiratory tract inflammation has recently been gained. In particular, the discovery of a complex network among cytokines, mediators and neuropeptides has offered the opportunity for advancing a new, integrative view of how the pathophysiological alterations responsible for respiratory allergic syndromes come about. We now realize that late phase allergic reactions, chronic allergic inflammation and tissue hyperreactivity are induced and maintained by a complex inflammatory mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)