Abstract
Reactive oxygen species (ROS) derived from the phagocyte NADPH oxidase (NOX2) are essential for host defence and immunoregulation. Their levels must be tightly controlled. ROS are required to prevent infection and are used in signalling to regulate several processes that are essential for normal immunity. A lack of ROS then leads to immunodeficiency and autoinflammation. However, excess ROS are also deleterious, damaging tissues by causing oxidative stress. In this review, we focus on two particular aspects of ROS biology: (i) the emerging understanding that NOX2-derived ROS play a pivotal role in the development and maintenance of adaptive immunity and (ii) the effects of excess ROS in systemic disease and how limiting ROS might represent a therapeutic avenue in limiting excess inflammation.
Highlights
1.1 Reactive Oxygen SpeciesReactive Oxygen Species (ROS) are small molecules that are derived from molecular oxygen
Increasing evidence has demonstrated that dysregulation of Reactive oxygen species (ROS) production can result in sustained inflammation and tissue damage which can be fatal during severe infection
It is important to further investigate the mechanisms underlying the regulation of ROS generation and how they become dysregulated during infection in order to understand how they may be targeted for clinical benefit in the future
Summary
Reactive Oxygen Species (ROS) are small molecules that are derived from molecular oxygen. They can either be classed as radicals or non-radicals, depending on whether they have an unpaired electron [1]. H2O2 is a very useful signalling molecule because it can be rapidly generated and rapidly removed via specific enzymes such as catalase, superoxide dismutase and peroxiredoxin enzymes. It can be quenched by non-enzymatic means such as glutathione (GSH) [3]. ROS generation can occur from many sources in cells These include mitochondria, peroxisomes and the P450 enzyme system. The NADPH oxidase is the first example of an enzyme where generating ROS is the primary function of the system, not a by-product of another process, e.g. the generation of ATP in mitochondria [discussed in [6]]
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