Intravenous immunoglobulin and atherosclerosis.
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 beta2-glycoprotein I (beta2-GPI). Immunoglobulin (Ig)G autoantibodies against beta2-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 atherosclerosis. The anti-atherogenic property of IVIg may be derived from non-antigen-specific antibody binding to FCgamma receptors, which blocks foam cell formation of macrophages. Several other possible mechanisms are also discussed.[1]References
- Intravenous immunoglobulin and atherosclerosis. Matsuura, E., Kobayashi, K., Inoue, K., Shoenfeld, Y. Clinical reviews in allergy & immunology. (2005) [Pubmed]
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