Th2 cells and GATA-3 in asthma: new insights into the regulation of airway inflammation.

Asthma is a clinical syndrome characterized by intermittent episodes of wheezing and coughing. The diagnosis is confirmed by abnormal lung physiology, including reversible airway obstruction and airways hyperresponsiveness (AHR). The pathologic manifestations of asthma include airway inflammation, airway remodeling, and mucus hypersecretion. Since the advent of bronchoscopy, we have been able to assess the lower airways in asthmatics during periods of disease activity and when the disease is quiescent and lung function is normal. From these studies, it has become clear that persistent inflammation is central to the pathogenesis of asthma. Bronchoscopic biopsies, bronchoalveolar lavage (BAL), and bronchoprovocation studies in patients with allergic asthma, intrinsic (nonallergic) asthma, or isocyanate-induced asthma show similar characteristic inflammatory responses. Increased numbers of inflammatory cells, predominantly eosinophils and lymphocytes, infiltrate the mucosa and submucosa in asthmatics independent of the etiology. It is now believed that airway inflammation leads to AHR (reviewed in ref. 1), airway remodeling (see article by Elias et al. in this series), and mucus hyperplasia (2, 3).