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The Journal of Immunology, 2002, 168: 705-712.
Copyright © 2002 by The American Association of Immunologists

Reduced Expression of Bcl-2 in CD8+ T Cells Deficient in the IL-15 Receptor {alpha}-Chain1

Tzong-Shoon Wu2,3,*, Jan-Mou Lee2,*,{dagger}, Yein-Gei Lai*,{dagger}, Jen-Chi Hsu*, Ching-Yen Tsai4,*, Ying-Hue Lee* and Nan-Shih Liao*,5,{dagger}

* Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan; and {dagger} Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan

Mice that lack IL-15 or the IL-15R {alpha}-chain (IL-15R{alpha}) 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-15R{alpha}-/- mice. The adult mutant mice exhibited a specific reduction in the percentage of CD8-single positive TCRhigh 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-15R{alpha}-/-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-15R{alpha} 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-15R{alpha}-/-mice.




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