ABSTRACT
Oxidative tissue damage is a hallmark of many chronic inammatory diseases, including atherosclerosis, fatty liver disease, type 2 diabetes, and autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis.1 The oxidatively modied molecules that accumulate in affected tissues include oxidized lipids, proteins, and nucleic acids, all of which have been suggested to contribute to the ongoing inammatory reaction.2 The importance of these molecules is highlighted by the fact that they are recognized by the immune system mainly in two ways: rst, there are germline encoded antibodies that recognize oxidized phospholipids;3 second, various immune and tissue cells respond to these molecules, partly by upregulating protective, antioxidant mechanisms,4 but also by inducing pro-inammatory responses, reminiscent of host-defense reactions.5 These reactions are considerably weaker than those in response to exogenous danger signals, such as those derived from invading microorganisms of bacterial or viral origin. Nevertheless, the similarity of the reactions evoked the thought that similar recognition mechanisms-in other words, the same receptors-might be involved.
