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传染病的一种常见免疫发病机制:蛋白质稳态系统假说。

A common immunopathogenesis mechanism for infectious diseases: the protein-homeostasis-system hypothesis.

作者信息

Lee Kyung-Yil

机构信息

Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea. ; Department of Pediatrics, The Catholic University of Korea, Daejeon St. Mary's Hospital, Daejeon, Korea.

出版信息

Infect Chemother. 2015 Mar;47(1):12-26. doi: 10.3947/ic.2015.47.1.12. Epub 2015 Mar 30.

Abstract

It was once believed that host cell injury in various infectious diseases is caused solely by pathogens themselves; however, it is now known that host immune reactions to the substances from the infectious agents and/or from the injured host cells by infectious insults are also involved. All biological phenomena in living organisms, including biochemical, physiological and pathological processes, are performed by the proteins that have various sizes and shapes, which in turn are controlled by an interacting network within the living organisms. The author proposes that this network is controlled by the protein homeostasis system (PHS), and that the immune system is one part of the PHS of the host. Each immune cell in the host may recognize and respond to substances, including pathogenic proteins (PPs) that are toxic to target cells of the host, in ways that depend on the size and property of the PPs. Every infectious disease has its own set of toxic substances, including PPs, associated with disease onset, and the PPs and the corresponding immune cells may be responsible for the inflammatory processes that develop in those infectious diseases.

摘要

曾经人们认为,各种传染病中宿主细胞损伤完全是由病原体自身造成的;然而,现在人们知道,宿主对感染因子的物质和/或感染性损伤导致的受损宿主细胞的物质产生的免疫反应也参与其中。生物体中的所有生物现象,包括生化、生理和病理过程,都是由具有各种大小和形状的蛋白质来执行的,而这些蛋白质又由生物体内的一个相互作用网络所控制。作者提出,这个网络由蛋白质稳态系统(PHS)控制,并且免疫系统是宿主PHS的一部分。宿主中的每个免疫细胞可能会根据致病蛋白(PPs)的大小和特性,以不同方式识别并对包括对宿主靶细胞有毒性的致病蛋白在内的物质做出反应。每种传染病都有其自身与疾病发作相关的一组有毒物质,包括致病蛋白,并且致病蛋白和相应的免疫细胞可能是那些传染病中发生的炎症过程的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a86e/4384454/3078f5dfba0c/ic-47-12-g001.jpg

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