ABSTRACT
T cell involvement in inflammatory airway conditions is perhaps most well characterized in allergic asthma [Herrick et al., 2003]. Asthma is a chronic inflammatory lung condition characterized by airway hyperreactivity and mucus hypersecretion. The clinical syndrome of asthma can be attributed to various etiologies and displays a variety of histopathologic properties. However, the bronchial mucosa of atopic asthmatics is unique due to characteristic lymphocyte and eosinophil infiltration. Other findings include goblet-cell hyperplasia and mucus plugging, bronchial smooth muscle hyperplasia and hypertrophy, subbasement membrane thickening and collagen deposition, and mast cell degranulation [Busse et al., 2001]. All of these findings work in concert to cause intermittent airway obstruction following allergen exposure. T cells were first implicated in the pathogenesis of asthma following the association of asthma severity with immunoglobulin E (IgE) antibodies [Burrows et al., 1989]. The initiation of IgE synthesis requires an adaptive immune response contingent on a specific T cell subset (Fig. 5.1). Upon inhalation of allergens, dendritic cells (DCs) lining the airway engulf and process antigens. DCs then migrate to draining lymph nodes, where they encounter T cells and B cells. Depending on the context in which DCs present antigen to T cells, a CD4+ T Helper 1 or 2 (TH1 or TH2) response is generated [Kim et al., 1985; Mosmann et al., 1986]. Each subset can be distinguished by a unique cytokine profile and has distinct effector functions.
