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脂氧素A4受体依赖性利什曼原虫感染

Lipoxin A4 receptor dependent leishmania infection.

作者信息

Wenzel Alexander, Van Zandbergen Ger

机构信息

Institute for Medical Microbiology and Hygiene, University Clinic of Ulm, Ulm, Albert Einstein Allee 11, D-89081, Germany.

出版信息

Autoimmunity. 2009 May;42(4):331-3. doi: 10.1080/08916930902828239.

Abstract

The lipoxin A4 receptor (ALX) is an important target of LxA4 in synovial tissues of patients with inflammatory arthritis. Previously this receptor was known as the FPRL-1 on PMN and shown to interact with acute phase proteins and a variety of peptides. ALX signalling can either activate or deactivate PMN functions. In this study, we found that both LxA4 and a chemotactic lipid leishmania chemotactic factor released by the parasite leishmania increased infectivity of this pathogen in an ALX dependent fashion. This functional characterization of ALX could lead to development of novel, therapeutic targets for treatment inflammatory diseases.

摘要

脂氧素A4受体(ALX)是炎症性关节炎患者滑膜组织中LxA4的重要靶点。此前该受体在中性粒细胞上被称为FPRL-1,并被证明可与急性期蛋白及多种肽相互作用。ALX信号传导可激活或失活中性粒细胞的功能。在本研究中,我们发现LxA4和寄生虫利什曼原虫释放的趋化脂质利什曼原虫趋化因子均以依赖ALX的方式增加该病原体的感染性。ALX的这一功能特性可能会为炎症性疾病的治疗带来新的治疗靶点。

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