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The exposure of susceptible individuals to environmental allergens induces enhanced levels of specific IgE antibodies, which bind to high affinity receptors on mast cells and basophils. Cross linking of receptor-bound IgE occurs, mediators are released and the immediate allergic reactions develop. Increased vascular permeability and the production of cytokines and chemokines cause polymorphonuclear granulocytes and lymphocytes to migrate into the site of allergic reactions and the late phase reaction is established. This illustrates that the cellular and cytokine networks activated in the pathogenesis of allergic inflammation are complex and involve many different cell types. However, the regulation of allergic immune responses in atopic individuals is mediated by cytokines characteristic of the Th2 functional phenotype (IL-4, IL-5, IL-10 and IL-13).1–5 In non-atopic individuals Thl cells, which produce IL-2 and IFN-γ, but not IL-4 or IL-5, are activated and regulate immune responses to allergens.6,7 However, from clonal analysis it is evident that Th0 cells, which have the potential to produce both Thl and Th2 cytokines, form a major component of the allergen specific repertoire in atopic individuals. Therefore, the ability to modify qualitative aspects of immune responses to allergens in atopic individuals by inhibiting the release of Th2 cytokines, and/or promoting the production of Thl cytokines may alter the clinical phenotype of some patients. The approach of immunotherapy mediated by peptides and designed to target allergen reactive CD4+ T cells are discussed in this report. |
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