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Antigen-induced airway hyperresponsiveness and airway inflammation are features of both human asthma and animal models of this disease. The genesis of these key asthma phenotypes represents the summation of a complex cascade of immune responses. It is hypothesized that multiple cell types are involved in the induction, propagation, and maintenance of these immune processes. Several molecules have been reported to be essential for cell-cell interactions, inflammatory cell recruitment, and effector functions leading to the overall expression of the asthmatic phenotype. This review summarizes the genetic evidence supporting a role for these molecules in antigen-driven airway hyperresponsiveness and inflammation.

Asthma is a disease characterized by intermittent airway obstruction, inflammatory cell infiltrates, increased mucus production, lung epithelial remodeling, and airway hyperreactivity. The genetics of asthma, as investigated in animal models, is poorly understood. Because no animal model of asthma mimics all of the pathologic and physiological features of asthma, genetic studies have focused on several phenotypes, including intrinsic or native airway hyperreactivity. It is generally accepted that both genetic and environmental factors determine the phenotypic expression of this complex disease. The genetics of airway hyperresponsiveness, as investigated in the mouse, are presented in this review. The inbred mouse currently represents the most valuable genetic resource for understanding the factors that control this complex phenotype.