Several inflammatory and immunological factors have been established as important contributors to atherogenesis. Among these, oxidized low-density lipoprotein (oxLDL) play a central role in the initiation and progression of atherosclerotic lesions. In atherosclerotic lesions, oxLDL was also found to co-localize with β2-glycoprotein I (β2-GPI). Immunoglobulin (Ig)G autoantibodies against β2-GPI complexed with oxLDL are pro-atherogenic because they increase uptake of the complexes by macrophages. In contrast, IgM natural anti-oxLDL antibodies derived from atherosclerosis-prone apolipoprotein E (ApoE) deficient mice reduced incidence of atherosclerosis. Such anti-oxLDL antibodies have been found in humans, and the accumulating evidences seem to support the idea that anti-oxLDL antibodies have a protective role for atherogenesis. Intravenous immunoglobulins (IVIgs) contain natural anti-oxLDL antibodies and infusion of IVIg into ApoE-deficient mice has been reported to decrease atheerosclerosis. The anti-atherogenic property of IVIg may be derived from non-antigen-specific antibody binding to FCγ receptors, which blocks foam cell formation of macrophages. Several other possible mechanisms are also discussed.
- Anti-oxLDL antibody
- Intravenous immunoglobulin (IVIg)
- Oxidized low-density lipoprotien (oxLDL)
- β-glycoprotein I (β-GPI)