Key result
CD59 deficiency accelerates atherosclerosis and premature death, mitigated by complement C5 inhibition in mice.
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Complement is a central effector system within the immune system and is implicated in a range of inflammatory disorders. CD59 is a key regulator of complement membrane attack complex (MAC) assembly. The atherogenic role of terminal complement has long been suspected but is still unclear. Here, we demonstrate that among mice deficient in apolipoprotein (Apo)E, the additional loss of murine CD59 (mCd59ab(-/-)/ApoE(-/-)) accelerated advanced atherosclerosis featuring occlusive coronary atherosclerosis, vulnerable plaque, and premature death and that these effect could be attenuated by overexpression of human CD59 in the endothelium. Complement inhibition using a neutralizing anti-mouse C5 antibody attenuated atherosclerosis in mCd59ab(-/-)/ApoE(-/-) mice. Furthermore, MAC mediated endothelial damage and promoted foam cell formation. These combined results highlight the atherogenic role of MAC and the atheroprotective role of CD59 and suggest that inhibition of MAC formation may provide a therapeutic approach for the treatment of atherosclerosis.
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Wu et al. (2009) studied Atherosclerosis. Loss of murine CD59 / Complement inhibition vs. ApoE(-/-) mice with intact CD59 was evaluated on Advanced atherosclerosis, vulnerable plaque, and premature death. CD59 deficiency in ApoE-deficient mice accelerated atherosclerosis and premature death, which was attenuated by human CD59 overexpression or neutralizing anti-mouse C5 antibody.
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