The immunology of atherothrombosis in the antiphospholipid syndrome: Antigen presentation and lipid intracellular accumulation
The immunology of atherothrombosis in the antiphospholipid syndrome: Antigen presentation and lipid intracellular accumulation
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DOI:
10.1016/j.autrev.2008.12.018
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发表时间:
2009-05-01
影响因子:
13.6
通讯作者:
Lopez, Luis R.
中科院分区:
文献类型:
--
作者:
Matsuura, Eiji;Kobayashi, Kazuko;Lopez, Luis R.
The antiphospholipid syndrome (APS), characterized by elevated serum levels of anti phospholipid antibodies (aPL) and thromboembolic complications, is a common cause of acquired hypercoagulability. The plasma protein beta 2-glycoprotein I (beta 2GPI) is the most clinically relevant antigenic target for aPL. Recent experimental evidence from our laboratory substantiated the concept that IgG anti-beta 2GPI immune complexes containing oxidized LDL (oxLDL) not only facilitated the intracellular accumulation of oxLDL in macrophages but also allowed the presentation of beta 2GPI epitopes to pathogenic autoreactive T cells. Both mechanisms required Fc gamma RI-mediated uptake by macrophages/monocytes. Furthermore, several clinical studies demonstrated that the presence of circulating oxLDL/beta 2GPI complexes and IgG autoantibodies to these complexes was significantly associated with vascular inflammation (i.e. autoimmune-mediated atherothrombosis) in autoimmune patients. In this article, we review recent findings concerning the biochemical and immunologic mechanisms involved in autoimmune-mediated atherothrombosis in patients with APS. (C) 2009 Elsevier B.V. All rights reserved.