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可溶性模式识别分子:气道黏膜表面稳态的守护者和调节剂。

Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces.

机构信息

Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.

出版信息

Eur J Immunol. 2020 May;50(5):624-642. doi: 10.1002/eji.201847811.

DOI:10.1002/eji.201847811
PMID:32246830
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7216992/
Abstract

Maintenance of homeostasis at body barriers that are constantly challenged by microbes, toxins and potentially bioactive (macro)molecules requires complex, highly orchestrated mechanisms of protection. Recent discoveries in respiratory research have shed light on the unprecedented role of airway epithelial cells (AEC), which, besides immune cells homing to the lung, also significantly contribute to host defence by expressing membrane-bound and soluble pattern recognition receptors (sPRR). Recent evidence suggests that distinct, evolutionary ancient, sPRR secreted by AEC might become activated by usually innocuous proteins, commonly referred to as allergens. We here provide a systematic overview on sPRR detectable in the mucus lining of AEC. Some of them become actively produced and secreted by AECs (like the pentraxins C-reactive protein and pentraxin 3; the collectins mannose binding protein and surfactant proteins A and D; H-ficolin; serum amyloid A; and the complement components C3 and C5). Others are elaborated by innate and adaptive immune cells such as monocytes/macrophages and T cells (like the pentraxins C-reactive protein and pentraxin 3; L-ficolin; serum amyloid A; and the complement components C3 and C5). Herein we discuss how sPRRs may contribute to homeostasis but sometimes also to overt disease (e.g. airway hyperreactivity and asthma) at the alveolar-air interface.

摘要

维持身体屏障的内稳态,这些屏障不断受到微生物、毒素和潜在生物活性(大)分子的挑战,需要复杂的、高度协调的保护机制。呼吸研究的最新发现揭示了气道上皮细胞 (AEC) 的前所未有的作用,除了归巢到肺部的免疫细胞外,AEC 通过表达膜结合和可溶性模式识别受体 (sPRR),对宿主防御也有重要贡献。最近的证据表明,AEC 分泌的独特的、进化古老的 sPRR 可能被通常无害的蛋白质(通常称为过敏原)激活。我们在此提供了对 AEC 黏液衬里中可检测到的 sPRR 的系统概述。其中一些由 AEC 主动产生和分泌(如 pentraxins C-reactive protein 和 pentraxin 3;collectins 甘露糖结合蛋白和表面活性剂蛋白 A 和 D;H-ficolin;血清淀粉样蛋白 A;以及补体成分 C3 和 C5)。其他由先天和适应性免疫细胞如单核细胞/巨噬细胞和 T 细胞产生(如 pentraxins C-reactive protein 和 pentraxin 3;L-ficolin;血清淀粉样蛋白 A;以及补体成分 C3 和 C5)。在此,我们讨论了 sPRR 如何有助于内稳态,但有时也会导致肺泡-空气界面的显性疾病(例如气道高反应性和哮喘)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eb0/7216992/ebf4e4a1044d/EJI-50-624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eb0/7216992/bddd1a67251f/EJI-50-624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eb0/7216992/ebf4e4a1044d/EJI-50-624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eb0/7216992/bddd1a67251f/EJI-50-624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eb0/7216992/ebf4e4a1044d/EJI-50-624-g002.jpg

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