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  • Title: Overexpression of interleukin-15 prevents the development of murine retrovirus-induced acquired immunodeficiency syndrome.
    Author: Umemura M, Nishimura H, Yajima T, Wajjwalk W, Matsuguchi T, Takahashi M, Nishiyama Y, Makino M, Nagai Y, Yoshikai Y.
    Journal: FASEB J; 2002 Nov; 16(13):1755-63. PubMed ID: 12409318.
    Abstract:
    LP-BM5 murine leukemia virus (MuLV) infection causes murine acquired immunodeficiency syndrome (MAIDS), a disease characterized by varied functional abnormalities of immunocompetent cells. We found that MAIDS progression was severely retarded in IL-15 transgenic (Tg) mice constructed with cDNA encoding secretable IL-15 under the control of an MHC class I promoter. Several immune defects, including impaired natural killer activity, depressed IFN-gamma production by T cells stimulated with anti-T cell receptor cross-linking, and increased susceptibility to Mycobacterium bovis infection, were prevented in IL-15 Tg mice inoculated with LP-BM5 MuLV. Cytotoxic T lymphocyte response to a highly antigenic 10-mer peptide encoded by LP-BM5-defective virus gag p12 gene was detected in the spleen and peritoneal exudate cells from IL-15 Tg mice infected with LP-BM5 MuLV. Intramuscular injection of cDNA encoding secretable IL-15 also prevented the development of MAIDS. These results indicate that IL-15 prevents the progression of MAIDS and may provide insight into an immunotherapeutic approach using the IL-15 gene for controlling retrovirus-induced immunodeficiency.
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