| First Author | Umemura M | Year | 2002 |
| Journal | FASEB J | Volume | 16 |
| Issue | 13 | Pages | 1755-63 |
| PubMed ID | 12409318 | Mgi Jnum | J:79951 |
| Mgi Id | MGI:2429327 | Doi | 10.1096/fj.02-0274com |
| Citation | Umemura M, et al. (2002) Overexpression of interleukin-15 prevents the development of murine retrovirus-induced acquired immunodeficiency syndrome. FASEB J 16(13):1755-63 |
| abstractText | 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. |
