Abstract
The inflammatory process in allergic disease is characterized by a distinct pattern of leukocyte accumulation, in particular increased numbers of activated eosinophils, T-lymphocytes, and monocytes with a relative paucity of neutrophils. Leukocyte migration through endothelium has been shown to be a staged process in which the cells are initially lightly tethered to the endothelium under flow conditions and roll along its surface. This is followed by cell activation, thought to be mediated by a soluble chemotactic stimulus that allows a firmer bond to develop between the leucocyte and the endothelial cell, which results in successful adhesion and transmigration (Fig. 1) (1). The steps occur in series so that each is essential for transmigration to occur. This means that selectivity can be introduced at each of the steps, resulting in considerable diversity in the pattern of signals at any one inflammatory site. It also means that migration can be modulated at each of the steps, offering a range of targets for pharmacological inhibition.
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Wardlaw, A. (1998). Adhesion Receptors in Allergic Disease. In: Denburg, J.A. (eds) Allergy and Allergic Diseases. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4757-2776-0_18
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DOI: https://doi.org/10.1007/978-1-4757-2776-0_18
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