Abstract
An animal model system was developed to study the mechanisms resulting in allergic sensitization. Local allergen exposure via the airways and the lung stimulated an allergen-specific immunoglobulin E (IgE) response that was paralleled by the development of increased airway responsiveness (AR). It was found that CD4+ T cells of local draining lymph nodes played an important role in the regulation of these events. Stimulation of allergen-specific T cells requires interaction between major histocompatibility complex (MHC) class II molecules (expressed on antigen-presenting cells), peptide (presented on MHC) and the T cell receptor. Allergen sensitization stimulated T cells that expressed a restricted T cell receptor V beta (TCR-V beta) elements. Each allergen stimulated different V beta elements, and sensitization to the same allergen resulted in a different pattern of TCR-V beta stimulation in different lymphoid tissues. Some of these T cells had pro-allergenic effects, whereas others were able to inhibit the development of the allergic response, including the development of increased AR. These data indicate that the local T cell response regulates the type of immune response that evolves following local allergen sensitization.

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