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纯化的人外周血嗜碱性粒细胞在免疫激活后会释放白细胞介素-13和预先形成的白细胞介素-4。

Purified human peripheral blood basophils release interleukin-13 and preformed interleukin-4 following immunological activation.

作者信息

Gibbs B F, Haas H, Falcone F H, Albrecht C, Vollrath I B, Noll T, Wolff H H, Amon U

机构信息

Department of Dermatology, Medical University of Lübeck, Germany.

出版信息

Eur J Immunol. 1996 Oct;26(10):2493-8. doi: 10.1002/eji.1830261033.

DOI:10.1002/eji.1830261033
PMID:8898965
Abstract

Recent studies have shown that human basophils, like mast cells, generate interleukin (IL)-4 following immunological activation and may thus participate in late-phase allergic and inflammatory processes. Here, we report the capacity of human basophils to release IL-13 within 24 h following stimulation with anti-IgE. Additionally, in 14 out of 31 experiments, we observed that basophils rapidly release performed IL-4 within 5-10 min, as well as newly generated IL-4, which was released 4 h following stimulation of the cells with anti-IgE. In contrast to the biphasic release of IL-4 from the cells, no preformed IL-13 was detected at earlier times (5-30 min). Preformed IL-4 and IL-4 and IL-13 generated de novo were also released after stimulation of the cells with IL-3; an enhanced production of these cytokines was observed using a combination of IL-3 and anti-IgE. We conclude from these data that, by releasing performed IL-4 and IL-4 and IL-13 generated de novo, human basophils may be centrally involved in the orchestration of allergic inflammation by providing a trigger to IL-4-mediated T helper 2 lymphocyte activation, B cell IgE switching, and increased vascular adhesion molecule expression.

摘要

最近的研究表明,人类嗜碱性粒细胞与肥大细胞一样,在免疫激活后会产生白细胞介素(IL)-4,因此可能参与迟发性过敏和炎症过程。在此,我们报告了人类嗜碱性粒细胞在抗IgE刺激后24小时内释放IL-13的能力。此外,在31项实验中的14项中,我们观察到嗜碱性粒细胞在5-10分钟内迅速释放已生成的IL-4,以及新生成的IL-4,后者在抗IgE刺激细胞4小时后释放。与细胞中IL-4的双相释放不同,在较早时间(5-30分钟)未检测到预先形成的IL-13。用IL-3刺激细胞后,预先形成的IL-4以及新生成的IL-4和IL-13也会释放;使用IL-3和抗IgE的组合观察到这些细胞因子的产生增加。从这些数据中我们得出结论,通过释放预先形成的IL-4以及新生成的IL-4和IL-13,人类嗜碱性粒细胞可能通过触发IL-4介导的辅助性T细胞2淋巴细胞激活、B细胞IgE转换和血管黏附分子表达增加,在过敏性炎症的协调中发挥核心作用。

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