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Inflammatory patterns in allergic rhinitis

机译:过敏性鼻炎的炎症模式

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Allergic rhinitis results from allergen-triggered early and late responses that are mediated by an array of inflammatory cells and mediators. Exposure to allergen induces the proliferation of T-helper type 2 (Th2) lymphocytes in allergic individuals leading to the subsequent release of a characteristic combination of cytokines that promotes IgE and mast cell production. Within the allergic epithelium, there is proliferation of mucosal mast cells that express IL-4, IL-5, IL-6 and tryptase. The resultant inflammatory mediators and cytokines enhance endothelial expression of adhesion molecules, such as vascular cell adhesion molecule-1. Chemoattractants, such as eotaxin, RANTES and IL-5, are responsible for the characteristic infiltration of the nasal mucosa by eosinophils, basophils, mast cells and Th2 lymphocytes that is seen in the late-phase allergic response. 2006 The Authors.
机译:过敏性鼻炎是由过敏原触发的早期和晚期反应引起的,这些反应是由一系列炎症细胞和介质介导的。接触变应原可诱导变态个体中T型辅助2型(Th2)淋巴细胞的增殖,从而导致随后释放促进IgE和肥大细胞生成的特征性细胞因子组合。在过敏性上皮内,有表达IL-4,IL-5,IL-6和类胰蛋白酶的粘膜肥大细胞增殖。所得的炎性介质和细胞因子增强粘附分子如血管细胞粘附分子-1的内皮表达。趋化因子,例如嗜酸性粒细胞趋化因子,RANTES和IL-5,是嗜酸性粒细胞,嗜碱性粒细胞,肥大细胞和Th2淋巴细胞在后期变态反应中可见的特征性鼻粘膜浸润。 2006作者。

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