| First Author | Lee TS | Year | 1999 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 19 |
| Issue | 3 | Pages | 734-42 |
| PubMed ID | 10073981 | Mgi Jnum | J:53839 |
| Mgi Id | MGI:1333550 | Doi | 10.1161/01.atv.19.3.734 |
| Citation | Lee TS, et al. (1999) The role of interleukin 12 in the development of atherosclerosis in ApoE-deficient mice. Arterioscler Thromb Vasc Biol 19(3):734-42 |
| abstractText | The cytokine profile of atherosclerotic aortas from apoE- deficient mice was assessed by reverse transcriptase- polymerase chain reaction. The results clearly showed that the expression of mRNA for IL-12p40 was evident in aortas from S-month-old apoE-deficient mice. The mRNA for IL-10 was detected in aorta from these mice at the age of 6 months, indicating that expression of IL-12 is earlier than that of IL-10 in these animals. Concurrent with IL- 12p40, the mRNA for the T-cell cytokine IFN-gamma, but not IL-4, was detected in aortas of mice at young and old ages. Both in situ hybridization and immunostaining further demonstrated the localization of IL-12 in macrophages of atherosclerotic lesions. Immunohistochemistry also demonstrated the expression of costimulatory molecules B7-1 and B7-2 in macrophages, suggesting that activation of T lymphocytes by macrophages may occur via surface antigens in lesions. When the immunoglobulin isotype of the antioxidized LDL antibodies in sera of apoE-deficient mice was determined, it revealed that both IgM and IgG were present. Furthermore, IgG2a is predominant and comprises approximate to 50% of the antioxidized LDL IgG in sera from young mice (3 months), but decreased to lower levels (35%) in older mice (6 months). Daily administration of IL-12 led to an increase in serum levels of antioxidized LDL antibodies and accelerated atherosclerosis in young apoE-deficient mice compared with control mice injected with PBS alone. Taken together, these data suggest that IL-12 plays an active role in regulating the immune response during the early phase of atherosclerosis in apoE-deficient mice. |
