Cited by 403Immune Response and InflammationAtherosclerosis and Cardiovascular DiseasesNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Innate sensing of oxidation-specific epitopes in health and disease

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Binder, Christoph J., Papac-Milicevic, Nikolina, Witztum, Joseph L.·2016·Nature Reviews Immunology

Abstract

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.

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Crossref · 10.1038/nri.2016.63

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  • The oxidation of lipids induces degradation products through lipid peroxidation, generating 4-HNE and MDA, which can modify protein function.

    “The oxidation of lipids induces degradation products through a process known as lipid peroxidation. This results in the generation of highly reactive products such as reactive aldehydes 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), which can modify protein function (Binder et al., 2016).”

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Authors
Binder, C. J., Papac-Milicevic, N., & Witztum, J. L.
Affiliations
  • Austrian Academy of Sciences (AT)
  • University of California San Diego (US)
Corresponding author
Binder, Christoph J.
Venue
Nature Reviews Immunology
Published
2016-06-27
Volume
16
Issue
8
Pages
485-497
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2468517437
Cited by
403
References
152
Citations by year
2026: 33 · 2025: 44 · 2024: 54 · 2023: 35 · 2022: 49 · 2021: 52 · 2020: 48 · 2019: 35 · 2018: 30 · 2017: 18 · 2016: 4 · 2014: 1
FWCI
2.76
Type
journal article
Language
en
Open access
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Austrian Science Fund (SFB‐54)
  • National Institutes of Health (HL055798)
  • National Heart, Lung, and Blood Institute (P01HL055798, R01HL119828, R01HL086559)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
oxidation-specific epitopes, lipid peroxidation, oxidative stress, damage-associated molecular patterns, innate immunity, pattern recognition receptors, chronic inflammation, atherosclerosis, age-related macular degeneration, tissue homeostasis, lipoprotein oxidation
MeSH terms
Animals, Epitopes, Disease Susceptibility, Homeostasis, Humans, Immunity, Cellular, Immunity, Innate, Oxidation-Reduction, Lipid Peroxidation, Oxidative Stress, Lipid Metabolism, Immunity, Humoral

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