静脉膜巨细胞与膜上皮进行通信,以调节免疫力
Kristin Westphalen1, Galina A Gusarova1, Mohammad N Islam1
1Lung Biology Laboratory, Department of Medicine, Division of Pulmonary, Allergy and Critical Care, Columbia University Medical Center, New York, New York 10032, USA.
Nature
|January 28, 2014
概括
居民气膜巨细胞 (AMs) 通过间隙结进行通信,以抑制肺炎. 这种新的途径,涉及连xin 43 (Cx43),可以防止过度的免疫反应和潜在的组织损伤在细菌感染期间.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 肺部医学 肺部医学
背景情况:
- 组织寄居的巨细胞对于屏障器官的宿主防御至关重要.
- 肺部的气膜巨细胞 (AMs) 作为防护者,对抗吸入的病原体.
- 由AMs启动的炎症反应可能会导致组织损伤,需要调节机制.
研究的目的:
- 为了研究膜巨细胞 (AMs) 如何调节炎症反应以防止肺组织损伤.
- 确定AMS使用的免疫调节的新机制.
主要方法:
- 实时现场膜成像被用来观察巨细胞与上皮细胞的相互作用.
- 评估了在AM中Connexin 43 (Cx43) 的表达和功能.
- 用AM特定的淘汰模式来研究Cx43.3的作用.
- 在炎症期间分析了 (Ca2+) 波传播和信号通路 (例如,Akt).
主要成果:
- 一个AMs的子集形成与膜上皮质的间隙连接通道,含有Cx43.
- 在脂聚糖诱导的炎症期间,这些AMs仍然附着并通过通过表皮通过同步的Ca2+波传递.
- 这种相互通信被发现具有免疫抑制作用,涉及Ca2+依赖的Akt激活.
- 在AM中Cx43的淘汰导致中性粒细胞的招募增加和促炎性细胞因子的分泌.
结论:
- 一种新的免疫调节机制存在,其中膜附着的AMs使用含有Cx43的间隙连接来传递免疫抑制信号.
- 这种AM-表皮沟通通道有助于减轻内毒素引起的肺炎,并防止过度组织损伤.
- 针对这种途径可以为炎症性肺部疾病提供新的治疗策略.
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