The T cell and the airway's fibrotic response in asthma

Abstract

From a clinical standpoint asthma presents as episodic airflow obstruction that is responsive to inhaled β2-adrenoceptor agonists. In more severe and persistent disease, asthma may progress to require an irreversible component, the mechanism(s) of which is not known. Two other important clinical features of asthma are bronchial hyperresponsiveness to a wide array of stimuli and clinical responsiveness of the disease to corticosteroids. The availability of bronchoalveolar lavage (BAL) and mucosal biopsy has helped tie these disparate aspects of asthma in demonstrating a special type of inflammation involving mast cells and eosinophils.1, 2 Accumulated evidence points to the T lymphocyte as a pivotal cell orchestrating the allergic inflammatory response. While the products from these cells and possibly the T cells themselves are capable of damaging the epithelium, other factors drive repair processes in the form of subepithelial fibrosis.