The cells and mediators of allergic inflammation

Abstract

SummaryIn sensitized atopic subjects allergen administration results in an immediate‐type reaction and, depending on the dose of the allergen, an additional late‐phase reaction. The early reaction results largely from the release of histamine, leukotrienes and other mediators from mast cells. The cutaneous late‐phase reaction is probably also predominantly mast‐cell‐dependent. The late asthmatic reaction, however, also involves T‐cell activation. T cells release a cascade of factors which evoke the migration of many cell types, including eosinophils, neutrophils and macrophages into the site of inflammation, under the influence of a complex combination of cytokines and chemokines. Neural inflammation (i.e. neuropeptides and neurotrophins) may also be involved. The identification of the processes underlying the inflammatory response to allergens, and their control mechanisms, provides specific targets for therapeutic measures (such as the use of monoclonal antibodies and soluble receptor molecules) which are designed to impede or abolish the allergic inflammatory cascade.