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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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The immunology of atherothrombosis in the antiphospholipid syndrome: antigen presentation and lipid intracellular accumulation.

The antiphospholipid syndrome (APS), characterized by elevated serum levels of antiphospholipid antibodies (aPL) and thromboembolic complications, is a common cause of acquired hypercoagulability. The plasma protein beta2-glycoprotein I (beta2GPI) is the most clinically relevant antigenic target for aPL. Recent experimental evidence from our laboratory substantiated the concept that IgG anti-beta2GPI immune complexes containing oxidized LDL (oxLDL) not only facilitated the intracellular accumulation of oxLDL in macrophages but also allowed the presentation of beta2GPI epitopes to pathogenic autoreactive T cells. Both mechanisms required FcgammaRI-mediated uptake by macrophages/monocytes. Furthermore, several clinical studies demonstrated that the presence of circulating oxLDL/beta2GPI 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.[1]

References

  1. The immunology of atherothrombosis in the antiphospholipid syndrome: antigen presentation and lipid intracellular accumulation. Matsuura, E., Kobayashi, K., Matsunami, Y., Lopez, L.R. Autoimmun. Rev (2009) [Pubmed]
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