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Atherogenic Antiphospholipid Antibodies in Antiphospholipid Syndrome
Author(s) -
KOBAYASHI KAZUKO,
LOPEZ LUIS R,
MATSUURA EIJI
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1422.052
Subject(s) - autoantibody , antiphospholipid syndrome , antibody , anticardiolipin antibodies , immunology , macrophage , chemistry , antigen , systemic lupus erythematosus , glycoprotein , medicine , biochemistry , in vitro , disease
: Macrophage uptake of oxidized LDL (oxLDL) plays a critical role in early stages of atherosclerosis. We previously reported that oxLDL forms stable complexes with β2‐glycoprotein I (β2GPI), and that these complexes were frequently present in the sera of patients with systemic lupus erythematosus (SLE) and/or antiphospholipid syndrome (APS). oxLDL/β2GPI complexes were shown to be antigenic targets for autoantibodies present in APS. To understand the role of autoantibodies in accelerated atherosclerosis of SLE and APS, we investigated the binding characteristics of β2GPI and oxLDL to mouse macrophages, and the effect of anti‐β2GPI and anti‐oxLDL autoantibodies on this macrophage binding. IgM anti‐oxLDL antibody (derived from Apoe −/– mouse) showed inhibitory effect on oxLDL binding to macrophages. Although β2GPI partly inhibited oxLDL binding to macrophages, IgG anti‐β2GPI autoantibody (derived from APS model mouse) showed pro‐atherogenic property by promoting the binding of oxLDL/β2GPI to macrophages .