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哮喘中调节嗜酸性粒细胞渗出的机制。

Mechanisms regulating eosinophil extravasation in asthma.

作者信息

Knol E F, Roos D

机构信息

Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, University of Amsterdam, The Netherlands.

出版信息

Eur Respir J Suppl. 1996 Aug;22:136s-140s.

PMID:8871059
Abstract

Infiltration of eosinophils into tissue allergic inflammation is mediated by a combination of processes. Eosinophil L-selection and very late activation antigen (VLA-4) can selectively regulate eosinophil adhesion to the endothelium. Activating cytokines, such as interleukin (IL)-5, regulated upon activation in normal T-cells (RANTES) and monocyte chemotactic peptide (MCP)-3 specifically act on eosinophils. Moreover, eosinophils from allergic individuals can be primed for increased adhesion and movement by chemokines released at sites of allergic inflammation. Together, these processes induce a specific infiltration of eosinophils.

摘要

嗜酸性粒细胞浸润到组织过敏性炎症是由多种过程共同介导的。嗜酸性粒细胞L-选择素和极迟活化抗原(VLA-4)可选择性调节嗜酸性粒细胞与内皮细胞的黏附。活化细胞因子,如白细胞介素(IL)-5、正常T细胞激活后调节的趋化因子(RANTES)和单核细胞趋化肽(MCP)-3可特异性作用于嗜酸性粒细胞。此外,来自过敏个体的嗜酸性粒细胞可被过敏性炎症部位释放的趋化因子致敏,从而增加黏附性和移动性。这些过程共同诱导嗜酸性粒细胞的特异性浸润。

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