Redox regulation of immunity and the role of small molecular weight thiols.
Redox regulation of immunity and the role of small molecular weight thiols.
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DOI：
10.1016/j.redox.2021.102001
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发表时间：
2021-08
期刊：
影响因子：
11.4
通讯作者：
Ghezzi P
中科院分区：
文献类型：
--
作者：
Ghezzi P
据认为，活性氧（ROS）的过度产生可能是许多疾病的原因，其中一些疾病具有炎症成分。这导致了一种过度简单化，即ROS被视为炎症和抗氧化剂抗炎。本文综述了巯基在宿主防御中的作用。该综述将首先总结我们在病原体感染中生存的机制。然后我们将考虑氧化还原领域如何从氧化应激的概念演变为氧化还原调节的概念，以及它如何与先天免疫领域交叉。第三部分将分析如何过度简化的氧化应激理论的疾病导致的假设的ROS和谷胱甘肽（GSH）在免疫中的作用，分别作为促炎和抗炎介质。最后，我们将讨论一些最近的研究，以及如何跳出这种过度简化的框框，将硫醇在氧化还原调节中的作用与我们在第一节中概述的感染中生存的机制联系起来。
It is thought that excessive production of reactive oxygen species (ROS) can be a causal component in many diseases, some of which have an inflammatory component. This led to an oversimplification whereby ROS are seen as inflammatory and antioxidants anti-inflammatory. This paper aims at reviewing some of the literature on thiols in host defense. The review will first summarize the mechanisms by which we survive infections by pathogens. Then we will consider how the redox field evolved from the concept of oxidative stress to that of redox regulation and how it intersects the field of innate immunity. A third section will analyze how an oversimplified oxidative stress theory of disease led to a hypothesis on the role of ROS and glutathione (GSH) in immunity, respectively as pro- and anti-inflammatory mediators. Finally, we will discuss some recent research and how to think out of the box of that oversimplification and link the role of thiols in redox regulation to the mechanisms by which we survive an infection outlined in the first section.
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DOI：
10.1186/cc5055
发表时间：
2006
期刊：
Critical care (London, England)
影响因子：
--
作者：
Cavaillon JM;Adib-Conquy M
通讯作者：
Adib-Conquy M
影响因子：
11.4
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Foresti, Roberta
影响因子：
4.4
作者：
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通讯作者：
Schumacker, PT
DOI：
10.1073/pnas.0500815102
发表时间：
2005-03-22
影响因子：
11.1
作者：
Dinkova-Kostova, AT;Liby, KT;Talalay, P
通讯作者：
Talalay, P
DOI：
10.1016/j.jtemb.2008.03.005
发表时间：
2008-01-01
影响因子：
3.5
作者：
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Zhong, Laifu