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  • Title: Atherosclerosis development in apolipoprotein E-null mice deficient for CD69.
    Author: Gómez M, Sanz-González SM, Abu Nabah YN, Lamana A, Sánchez-Madrid F, Andrés V.
    Journal: Cardiovasc Res; 2009 Jan 01; 81(1):197-205. PubMed ID: 18703531.
    Abstract:
    AIMS: Atherosclerosis is a chronic inflammatory disease regulated by immune mechanisms. CD69 is a cell surface receptor rapidly induced after leukocyte activation at sites of chronic inflammation. Genetic disruption of CD69 in the mouse aggravates collagen-induced arthritis (CIA), and partial depletion of CD69-expressing cells with anti-CD69 monoclonal antibody (mAb) prevents CIA development in wild-type mice, suggesting that this receptor negatively modulates immune and inflammatory responses. It has been recently reported that CD69 is upregulated in a large subset of T cells in atherosclerosis-prone apolipoprotein E-null mice (apoE(-/-)). In this study, we investigated whether altering CD69 function affects atherosclerosis development. METHODS AND RESULTS: We studied native and diet-induced atherosclerosis in apoE(-/-) and doubly deficient apoE(-/-)CD69(-/-) mice and performed expression studies in tissues and primary cells derived from these animals. Plasma cholesterol level was unaffected by CD69 genetic inactivation. Although this genetic manipulation led to an elevated production of interferon gamma and interleukin 10 by activated T cells, apoE(-/-) and apoE(-/-)CD69(-/-) mice fed control and high-fat diet exhibited atheromas of similar size and composition when analysed at different stages of the disease. Likewise, anti-CD69 mAb treatment had no effect on plasma cholesterol and atherosclerosis burden in fat-fed apoE(-/-) mice. CONCLUSION: In contrast to previous studies highlighting the protective function of CD69 against CIA, an autoimmune inflammatory disease, our results rule out a significant role for CD69 against atherosclerosis in apoE(-/-) mice, an experimental disease model featuring a local inflammatory response triggered and sustained by alterations in lipid homeostasis.
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