作者: Alistair J. Ramsay , Simon P. Hogan , Paul S. Foster , Yelin Xiong
DOI: 10.1007/978-3-0348-8478-5_5
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摘要: Although the chain of events leading to asthma is highly complex, dysregulated production type 2 cytokines, notably IL-4 and IL-5, by allergen-specific T cells, has emerged as an important causative factor [1, 2]. The symptoms allergic asthma, including reversible airways occlusion hyperreactivity (AHR), correlate with a local infiltration mucosa inflammatory whose recruitment activation influenced IL-3, IL-4, granulocyte-macrophage colony stimulating other chemotactic agents produced activated Th2 cells [3-6]. Indeed, severity disease appears degree inflammation level cell activity [7, 8]. molecular cellular mechanisms underlying presence large numbers in remain be resolved, however their products appear have profound specific effects promoting disease. for example, regulates all stages development eosinophils, which are consistently predominant leukocyte population infiltrate asthmatics [5]. modulates mast [4] and, through its influence on Ig class switching, IgE [3] may specifically sensitize implicated disease, basophils macrophages. This leads release substances histamine, leukotrienes, platelet-activating factor, cationic proteins chemokines may, turn, augment process.