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Intravenous immunoglobulin and atherosclerosis

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Abstract

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.

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Authors and Affiliations

  1. Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan

    Eiji Matsuura & Kazuko Kobayashi

  2. Department of Cardiovascular Medicine, Kurashiki Central Hospital, Kurashiki, Japan

    Katsumi Inoue

  3. Department of Medicine B, Sheba Medical Center, Tel-Hashomer, Israel

    Yehuda Shoenfeld

  4. Incombent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases, Tel Aviv University, Tel Aviv, Israel

    Yehuda Shoenfeld

Authors
  1. Eiji Matsuura
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  2. Kazuko Kobayashi
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  3. Katsumi Inoue
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  4. Yehuda Shoenfeld
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Correspondence to Eiji Matsuura.

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Matsuura, E., Kobayashi, K., Inoue, K. et al. Intravenous immunoglobulin and atherosclerosis. Clinic Rev Allerg Immunol 29, 311–319 (2005). https://doi.org/10.1385/CRIAI:29:3:311

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  • DOI: https://doi.org/10.1385/CRIAI:29:3:311

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