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Innate sensing of oxidation-specific epitopes in health and disease
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Innate sensing of oxidation-specific epitopes in health and disease
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Journal Article
Innate sensing of oxidation-specific epitopes in health and disease
2016
Overview
Key Points
Oxidative stress results in the oxidative damage of membrane lipids, leading to the formation of neo-self epitopes, which are known as oxidation-specific epitopes (OSEs).
Major carriers of OSEs are dying cells, microvesicles and damaged proteins and lipoproteins, such as oxidized low-density lipoproteins.
OSEs are recognized by multiple arcs of the innate immune system, such as soluble pattern recognition receptors (natural antibodies and complement components) and cellular pattern recognition receptors (Toll-like receptors and scavenger receptors).
OSEs have an important role in physiological processes by serving as markers of oxidatively modified endogenous structures, allowing the immune system to mediate their clearance and to maintain homeostasis.
The accumulation of OSEs can trigger sterile inflammation.
OSEs have been suggested to contribute, as drivers of disease development, to various chronic and acute inflammatory diseases, including atherosclerosis, non-alcoholic steatohepatitis and age-related macular degeneration.
Oxidation-specific epitopes (OSEs) function as markers of oxidative damage of membrane lipids. This Review discusses the immune recognition of OSEs, as well as their role in the maintenance of tissue homeostasis and their contribution to the development of inflammatory diseases.
Ageing, infections and inflammation result in oxidative stress that can irreversibly damage cellular structures. The oxidative damage of lipids in membranes or lipoproteins is one of these deleterious consequences that not only alters lipid function but also leads to the formation of neo-self epitopes — oxidation-specific epitopes (OSEs) — which are present on dying cells and damaged proteins. OSEs represent endogenous damage-associated molecular patterns that are recognized by pattern recognition receptors and the proteins of the innate immune system, and thereby enable the host to sense and remove dangerous biological waste and to maintain homeostasis. If this system is dysfunctional or overwhelmed, the accumulation of OSEs can trigger chronic inflammation and the development of diseases, such as atherosclerosis and age-related macular degeneration. Understanding the molecular components and mechanisms that are involved in this process will help to identify individuals with an increased risk of developing chronic inflammation, and will also help to indicate novel modes of therapeutic intervention.
