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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Annu Rev Pathol. 2013 Aug 7;9:73–102. doi: 10.1146/annurev-pathol-020712-163936

Figure 1.

Figure 1

Summary of oxidation-specific epitopes (OSEs) as major antigens of innate immunity. Oxidation-induced changes in normal self-molecules generate OSEs that are recognized as damage-associated molecular patterns (DAMPs) by the innate immune system. OSEs are also found on apoptotic cells and on microbes (or molecular mimics), where they serve as pathogen-associated molecular patterns (PAMPs). Oxidation of low-density lipoprotein (LDL), which occurs in atherosclerotic lesions, generates several OSEs, such as exposed phosphocholine (PC), malondialdehyde (MDA), oxidized cardiolipin (OxCL), and 4-hydroxynonenal (4HNE). These DAMPs are recognized by various pattern recognition receptors (PRRs) of the innate immune system. For example, PC on OxLDL, apoptotic cells, and Streptococcus pneumoniae is recognized by the innate immunoglobulin M (IgM) natural antibody (NAb) E06, the scavenger receptors (SRs) CD36 and SR-B1, and the pentraxin C-reactive protein (CRP). MDA is recognized by the NAbs E014 and NA17, SR-A, and complement factor H (CFH). An MDA mimic recognized by E014 is found on group A Streptococcus. These OSEs and others are present in atherosclerotic lesions and act as major antigens stimulating innate and adaptive responses that affect the progression of vascular disease.