ABSTRACT
Asthma is a clinical syndrome caused by chronic bronchial in£ammation, reversible airway obstruction, and airway hyperresponsiveness (AHR). A number of factors, such as allergens, irritants, or infections, which induce or exacerbate in£ammation of the airways, may play a role in initiating asthma. Allergic or extrinsic asthma is an in£ammatory-mediated disease characterized by in¢ltration of the airways by T lymphocytes, mast cells, and eosinophils in response to inhalation of ubiquitous aeroallergens (1). Analysis of bronchoscopic biopsies and bronchoalveolar lavage (BAL) samples taken from allergic asthmatics revealed that CD4þ T cells expressing an activated memory Th2 phenotype are the predominant lymphocyte population. These cells expressed elevated levels of mRNA for the cytokines interleukin-4 (IL-4), IL-5, IL-13, and granulocyte-macrophage colony-stimulating factor (GM-CSF), indicating that have play a role in initiating and sustaining allergic in£ammation (2,3). The reason only a proportion of atopic individuals develop asthma in response to inhalation of allergens is not fully understood. The mucosal surfaces of the airways are continually exposed to substances from the environment, and the immune system has evolved mechanisms to distinguish between pathogenic and innocuous substances. In most individuals, soluble proteins delivered to the nasal mucosa do not invoke an immune response but induce a state of nonresponsiveness, or tolerance, to the antigen. There has been considerable interest in understanding the mechanisms involved in the induction and maintenance of
mucosal tolerance to inhaled antigen and in exploiting this as a therapeutic approach for preventing pathogenic responses to inhaled allergens (4).
