Oxidation-specific epitope (OSE)

Oxidation-specific epitopes are neoepitopes generated when endogenous biomolecules (such as lipids, proteins, and lipoproteins) undergo oxidative modification by reactive oxygen species, often as a result of inflammation, metabolic stress, or aging. They are not individual molecules but a heterogeneous set of oxidized molecular structures (such as oxidized phospholipids, malondialdehyde adducts, oxidized cholesteryl esters) that signal cellular or tissue damage. OSEs are recognized by several pattern recognition receptors (PRRs) of the innate immune system, including scavenger receptors (e.g., CD36), toll-like receptors, natural antibodies, and C-reactive protein. Their recognition mediates the clearance of apoptotic cells and damaged debris and can trigger inflammation. Accumulation of OSEs, or disturbed recognition/clearance, has been implicated in the pathogenesis of chronic inflammatory diseases particularly atherosclerosis, as well as in non-alcoholic steatohepatitis and other conditions. OSEs are thus best understood as immunologically relevant oxidation-derived patterns, not as druggable molecular targets.

Other names

OSEoxidation-specific epitopesoxidized neoepitopesDAMPs (as a subset of damage-associated molecular patterns)

Neutralization of OSEs (by antibodies or immune components); Blockade of OSE recognition by pattern recognition receptors (theoretical/experimental)