[Recent data on the physiopathology of respiratory allergies]

Mechanisms of the allergic inflammatory reaction in the respiratory tract, such as those involved in chronic asthma and allergic rhinitis involve a complex and integrated cellular cascade. After allergen inhalation, the response is initiated by the airway epithelial dendritic cells which are responsible after transportation to regional lymph nodes, for the presentation to naïve CD4+ T helper (Th0) cells. After the first phase of allergen sensitization, CD4+ T cells give rise in atopic patients to lymphocytes CD4+ with a cytokine profile of Th2-type (secretion of IL-4, IL-5 and IL-13). Both cytokines IL-4 and IL-13 favor the IgE antibody production towards inhaled allergens, while IL-5 allows the differentiation, activation and survival of eosinophils. Among effector cells, two are predominant: mast-cells and activated eosinophils. During the initiation phase of the allergic reaction the dominant phenomena is represented by IgE mediated mast cell/basophil activation which leads to the release of granular mast cell mediators but also to the secretion by mast cells of cytokines also offering a Th2 profile. Moreover in chronic asthma histopathological, immunocytochemical studies and in situ hybridization techniques demonstrate a large recruitment of inflammatory cells, mainly of activated eosinophils that similarly produce Th2 type cytokines and participate in the development of the local allergic inflammation. Several additive environmental factors such as viruses or aeropollutants are susceptible to amplify the Th2 type response; conversely specific immunotherapy has been shown to allow a shift from the Th2 to Th1 profile, which explains at least for a part its therapeutic effects.