ABSTRACT
While it is generally accepted that mast cell activation is critical for the expression of the acute bronchoconstriction provoked by allergen challenge in subjects with atopic asthma, there is much less agreement about the roles of mast cells in the late phase reactions or chronic allergic inflammation associated with this disorder (reviewed in Refs. 1-6). In this chapter we shall discuss the characteristics of the mast cell that enable it to act as both an important effector cell and as a potential immunoregulatory cell in asthma and other allergic diseases. Although many potential mechanisms may contribute to mast cell activation in subjects with asthma, including those involving complement (7,8), neurotrophins, or neuropeptides (9-11), the c-kit ligand stem cell factor (12-14), T-cell-derived products (15), and products of bacteria or viruses (16-18) (see other chapters in this volume), we shall focus on the role of IgE in eliciting mast cell function in this setting. We shall present evidence, much of it derived from in vivo studies in mice, indicating that mast cells can indeed contribute importantly to the expression of IgE-dependent late phase reactions, IgE-dependent enhancement of airway hyperreactivity and certain features of chronic allergic inflammation in the airways. As a subtheme, we shall consider two important issues that contribute to the “controversy” about the relevance of the findings obtained in murine asthma “models” to our understanding of asthma in
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humans: the redundancy and complexity of effector and immunoregulatory mechanisms in IgE-associated immune responses and certain differences in these processes in mice and humans.
