| First Author | Wu TS | Year | 2002 |
| Journal | J Immunol | Volume | 168 |
| Issue | 2 | Pages | 705-12 |
| PubMed ID | 11777964 | Mgi Jnum | J:73738 |
| Mgi Id | MGI:2156338 | Doi | 10.4049/jimmunol.168.2.705 |
| Citation | Wu TS, et al. (2002) Reduced expression of Bcl-2 in CD8+ T cells deficient in the IL-15 receptor alpha-chain. J Immunol 168(2):705-12 |
| abstractText | Mice that lack IL-15 or the IL-15R alpha-chain (IL-15Ralpha) are deficient in peripheral CD8(+), but not in CD4(+), T cells. This CD8(+) T cell-specific deficiency has now been investigated further by characterization of a new strain of IL-15Ralpha(-/-) mice. The adult mutant mice exhibited a specific reduction in the percentage of CD8-single positive TCR(high) thymocytes. The expression of Bcl-2 was reduced in both CD8(+) thymocytes and naive T cells of the mutant animals, and the susceptibility of these cells to death was increased. Memory CD8(+) cells were profoundly deficient in IL-15Ralpha(-/-)mice, and the residual memory-like CD8(+) cells contained a high percentage of dead cells and failed to up-regulate Bcl-2 expression compared with naive CD8(+) cells. Moreover, exogenous IL-15 both up-regulated the level of Bcl-2 in and reduced the death rate of wild-type and mutant CD8(+) T cells activated in vitro. These results indicate that IL-15 and IL-15Ralpha regulate the expression of Bcl-2 in CD8(+) T cells at all developmental stages. The reduced Bcl-2 content in CD8(+) cells might result in survival defect and contribute to the reduction of CD8(+) cells in IL-15Ralpha(-/-)mice. |
