Eosinophils and allergy in asthma.

S Makino, T Fukuda
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引用次数: 24

Abstract

Eosinophils are recruited to the site of IgE-mediated allergic reaction in the airway in asthma. Major eosinophil-chemotactic factors released from mast cells are platelet activating factor and Leukotriene B4. In addition, T cells and bronchial epithelial cells produce eosinophil chemotactic cytokines. Cytokines including IL-5, IL-3, and GM-CSF, which are released mainly from CD4+ T cells and possibly Th2, activates eosinophils for migration, tissue damage, and survival. Adhesion molecules on eosinophils and constituent structures of the airway participate in the process of eosinophil migration. Among a variety of adhesion molecules, VLA-4 and VCAM-1 are unique to the interaction between eosinophils and endothelial cells. A major role of recruited eosinophils in the airway in asthma is considered to be damage to the bronchial epithelium caused by eosinophil specific granules proteins, in addition to production of lipid mediators, production of cytokines, antigen-presenting cell function, and possible induction of basement membrane thickening in the airway.

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哮喘中的嗜酸性粒细胞和过敏。
嗜酸性粒细胞被募集到哮喘气道中ige介导的过敏反应部位。肥大细胞释放的嗜酸性趋化因子主要有血小板活化因子和白三烯B4。此外,T细胞和支气管上皮细胞产生嗜酸性趋化细胞因子。细胞因子包括IL-5、IL-3和GM-CSF,主要由CD4+ T细胞和可能的Th2释放,激活嗜酸性粒细胞迁移、组织损伤和生存。嗜酸性粒细胞的粘附分子和气道的组成结构参与了嗜酸性粒细胞迁移的过程。在众多粘附分子中,vca -4和VCAM-1是嗜酸性粒细胞与内皮细胞相互作用所特有的。在哮喘气道中,嗜酸性粒细胞募集的主要作用被认为是由嗜酸性粒细胞特异性颗粒蛋白引起的支气管上皮损伤,除了产生脂质介质,产生细胞因子,抗原呈递细胞功能,并可能诱导气道基底膜增厚。
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