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人类嗜酸性粒细胞凋亡的药理学调控

Pharmacological regulation of human eosinophil apoptosis.

作者信息

Kankaanranta Hannu, Moilanen Eeva, Zhang Xianzhi

机构信息

The Immunopharmacology Research Group, Medical School, FIN-33014, University of Tampere and Department of Respiratory Medicine, Tampere, Finland.

出版信息

Curr Drug Targets Inflamm Allergy. 2005 Aug;4(4):433-45. doi: 10.2174/1568010054526395.

DOI:10.2174/1568010054526395
PMID:16101520
Abstract

Eosinophilic inflammation of the airways is a key characteristic of asthma. The balance between eosinophil recruitment into the lung and their removal from the lungs determines the number of eosinophils in the airways. Apoptosis or programmed cell death is of importance in the removal of eosinophils from the lungs. In asthma, eosinophil apoptosis is delayed. Glucocorticoids enhance eosinophil apoptosis, whereas beta(2)-agonists may delay apoptosis in eosinophils. Detailed knowledge on the mechanisms that regulate this process gives an opportunity to develop specific asthma therapies targeting the eosinophil. This review aims to focus on the signalling leading to or preventing apoptosis in human eosinophils as well as reviews the current evidence on the regulation of eosinophil apoptosis and/or survival in allergic diseases.

摘要

气道嗜酸性粒细胞炎症是哮喘的关键特征。嗜酸性粒细胞募集到肺与从肺中清除之间的平衡决定了气道中嗜酸性粒细胞的数量。凋亡或程序性细胞死亡在从肺中清除嗜酸性粒细胞方面具有重要意义。在哮喘中,嗜酸性粒细胞凋亡延迟。糖皮质激素可增强嗜酸性粒细胞凋亡,而β2激动剂可能会延迟嗜酸性粒细胞的凋亡。对调节这一过程的机制的详细了解为开发针对嗜酸性粒细胞的特异性哮喘治疗方法提供了机会。本综述旨在关注导致或阻止人类嗜酸性粒细胞凋亡的信号传导,以及综述目前关于过敏性疾病中嗜酸性粒细胞凋亡和/或存活调节的证据。

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