Linked Life Data

10073981

Source:http://linkedlifedata.com/resource/pubmed/id/10073981

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pubmed-article:10073981pubmed:abstractTextThe 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 3-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 approximately 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.lld:pubmed
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pubmed-article:10073981pubmed:articleTitleThe role of interleukin 12 in the development of atherosclerosis in ApoE-deficient mice.lld:pubmed
pubmed-article:10073981pubmed:affiliationDivision of Cardiovascular Research, Institute of Biomedical Sciences, Academia Sinica, Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.lld:pubmed
pubmed-article:10073981pubmed:publicationTypeJournal Articlelld:pubmed
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