Accumulation in tissues of subsets of leukocytes, especially eosinophils, basophils, and Th2 lymphocytes, is a hallmark of asthma and other forms of chronic allergic inflammation (1,2). The notion that these cells play central roles in allergic diseases is supported by the identification of their mediators at sites of allergic inflammatory responses and the reduction of these cells and their mediators during the resolution of allergic reactions (reviewed in Ref. 3). Selective migration of these cells also occurs following the instillation of allergen into the airways during human experimental late phase responses (LPRs). For example, eosinophils can account for 60% or more of the cells entering the lumen of the lower airways after introduction of allergen by segmental challenge (4). Basophil numbers in the lower airway also increase during the LPR, often by more than 100-fold, and can account for as many as 3% of the total infiltrating cells (5). The vast majority of infiltrating T cells in the lung are CD4memory cells displaying a cytokine pattern typical for Th2 cells, including production of IL-4 and IL-5 (1).
|Original language||English (US)|
|Title of host publication||Therapeutic Targets in Airway Inflammation|
|Number of pages||26|
|State||Published - Jan 1 2003|
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