ABSTRACT
In the majority of patients, asthma appears to be mediated by an immune response to allergen resulting in pulmonary inflammation and bronchial or airway hyperreactivity (AHR). Data from clinical studies of asthma patients and animal models of allergic pulmonary inflammation have shown that both T cells and inflammatory cells, especially eosinophils, are essential in the initiation and progression of the lung pathology. Mast cells mediate effector function through binding of allergenspecific immunoglobulin E (IgE), resulting in degranulation and release of numerous mediators, including cytokines and chemokines. On the other hand, IgE-dependent mast cell (and basophil) activities in human disease may be more relevant in the early phase response and less critical for sustaining long-term, chronic inflammation or airway remodeling. In contrast, T lymphocytes and eosinophils play significant roles in the progression of chronic inflammation and changes in airway function.
