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- W1971248032 abstract "It has been known for many years that individuals with autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are at increased risk of cardiovascular disease1,2. While it is unclear whether the presence of autoantibodies is responsible for the increased risk, such a possibility seems inherently plausible since at least some autoantibodies (such as lupus anticoagulant and antiphospholipid antibodies, but also more recently anti-hsp60 antibodies3) are known to modulate clotting cascades and are associated with increased risk of thrombus formation. In parallel, it has been known since the 1980s that autoantibodies against oxidized lipoprotein epitopes are prevalent in subjects with clinically significant atherosclerosis4. There are several possible causes of such an association: lipid oxidation is more common among individuals with atherosclerosis, so increased presence of the epitope could increase prevalence of antibodies. Alternatively, changes in immune system regulation associated with a systemic proinflammatory status might increase the likelihood of an autoimmune response against oxidized lipoproteins, or indeed against other self-antigens such as heat shock proteins. Irrespective of the pathways responsible, these autoantibodies associated with atherosclerosis could merely mark processes that are pathogenic, or they could themselves modulate disease progression. There is considerable debate as to the role of such autoantibodies, with the possibility that IgG against oxidized low density lipoprotein (LDL) are pathogenic while IgM antibodies against similar epitopes are protective5 … Address correspondence to Dr. Grainger. E-mail: djg15{at}cam.ac.uk" @default.
- W1971248032 created "2016-06-24" @default.
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- W1971248032 date "2009-11-01" @default.
- W1971248032 modified "2023-09-28" @default.
- W1971248032 title "When Worlds Collide: Autoimmunity and Atherosclerosis" @default.
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- W1971248032 doi "https://doi.org/10.3899/jrheum.091027" @default.
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