| First Author | Nicoletti A | Year | 1998 |
| Journal | J Clin Invest | Volume | 102 |
| Issue | 5 | Pages | 910-8 |
| PubMed ID | 9727059 | Mgi Jnum | J:49660 |
| Mgi Id | MGI:1277802 | Doi | 10.1172/JCI119892 |
| Citation | Nicoletti A, et al. (1998) Immunoglobulin treatment reduces atherosclerosis in apo E knockout mice. J Clin Invest 102(5):910-8 |
| abstractText | Atherosclerosis is associated with immune activation. T cells and macrophages infiltrate atherosclerotic plaques and disease progression is associated with formation of autoantibodies to oxidized lipoproteins. In the apo E knockout mouse, a genetic model of cholesterol-induced atherosclerosis, congenital deficiency of macrophages, lymphocytes, or interferon-gamma receptors result in reduced lesion formation. We have now evaluated whether immune modulation in the adult animal affects disease development. Injections of 7-wk-old male apo E knockout mice with polyclonal immunoglobulin preparations (ivIg) during a 5-d period reduced fatty streak formation over a 2-mo period on cholesterol diet by 35%. Fibrofatty lesions induced by diet treatment for 4 mo were reduced by 50% in mice receiving ivIg after 2 mo on the diet. ivIg treatment also reduced IgM antibodies to oxidized LDL and led to inactivation of spleen and lymph node T cells. These data indicate that ivIg inhibits atherosclerosis, that it is effective both during the fatty streak and plaque phases, and that it may act by modulating T cell activity and/or antibody production. Therefore, immunomodulation may be an effective way to prevent and/or treat atherosclerosis. |
