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正常和HIV感染受试者B细胞中的趋化性及白细胞介素-8受体表达

Chemotaxis and IL-8 receptor expression in B cells from normal and HIV-infected subjects.

作者信息

Jinquan T, Møller B, Storgaard M, Mukaida N, Bonde J, Grunnet N, Black F T, Larsen C G, Matsushima K, Thestrup-Pedersen K

机构信息

Department of Dermatology, University Hospital, Aarhus University, Denmark.

出版信息

J Immunol. 1997 Jan 1;158(1):475-84.

PMID:8977225
Abstract

To date, the activities of the alpha chemokines for human peripheral B cells from normal subjects (N-B cells) or from HIV-infected subjects (HIV-B cells) are not well established. No report on the IL-8R expression on N-B cells and HIV-B cells has been seen. We report in this work that the alpha chemokines IL-8 and growth-regulatory oncogene-alpha (GRO-alpha) induce a chemotactic migration of N-B cells and HIV-B cells via stimulating the IL-8RB on these cells. The chemotaxis of N-B cells can be inhibited by IFN-gamma and IL-2, and augmented by IL-4 and IL-13, whereas TNF-alpha and IL-10 have no influence. The chemotaxis of HIV-B cells can be inhibited by IFN-gamma and IL-2, and augmented by TNF-alpha, IL-4, and IL-10, whereas IL-13 has no influence. IL-8R are expressed more abundantly on freshly isolated HIV-B cells than N-B cells (51% and 15%, respectively). The IL-8R on N-B cells can be down-regulated by IFN-gamma, IL-2, and TNF-alpha (selectively on IL-8RA), and up-regulated by IL-4 and IL-13, whereas IL-10 has no influence. The IL-8R on HIV-B cells can be down-regulated by IFN-gamma and IL-2, and up-regulated by TNF-alpha, IL-4, and IL-10, whereas IL-13 has no influence. Importantly, N-B cell and HIV-B cell chemotaxis toward IL-8 and GRO-alpha can be blocked by anti-IL-8RB polyclonal Ab, but not by anti-IL-8RA polyclonal Ab. Our results demonstrate that IL-8 and GRO-alpha are important inflammatory mediators that stimulate the directional migration and recruitment of B lymphocytes. The migratory behavior and the expression of IL-8R on HIV-B cells and some of the reactions to Th1- and Th2-like cytokines are modified significantly during HIV infection.

摘要

迄今为止,α趋化因子对正常受试者(N-B细胞)或HIV感染受试者(HIV-B细胞)的人外周血B细胞的活性尚未完全明确。尚未见到关于N-B细胞和HIV-B细胞上IL-8R表达的报道。我们在这项研究中报告,α趋化因子IL-8和生长调节致癌基因-α(GRO-α)通过刺激这些细胞上的IL-8RB诱导N-B细胞和HIV-B细胞发生趋化性迁移。N-B细胞的趋化作用可被IFN-γ和IL-2抑制,被IL-4和IL-13增强,而TNF-α和IL-10则无影响。HIV-B细胞的趋化作用可被IFN-γ和IL-2抑制,被TNF-α、IL-4和IL-10增强,而IL-13则无影响。新鲜分离的HIV-B细胞上IL-8R的表达比N-B细胞更丰富(分别为51%和15%)。N-B细胞上的IL-8R可被IFN-γ、IL-2和TNF-α(选择性作用于IL-8RA)下调,被IL-4和IL-13上调,而IL-10则无影响。HIV-B细胞上的IL-8R可被IFN-γ和IL-2下调,被TNF-α、IL-4和IL-10上调,而IL-13则无影响。重要的是,N-B细胞和HIV-B细胞对IL-8和GRO-α的趋化作用可被抗IL-8RB多克隆抗体阻断,但不能被抗IL-8RA多克隆抗体阻断。我们的结果表明,IL-8和GRO-α是刺激B淋巴细胞定向迁移和募集的重要炎症介质。在HIV感染期间,HIV-B细胞的迁移行为和IL-8R的表达以及对Th1样和Th2样细胞因子的一些反应发生了显著改变。

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