Memory-type CD8+ T cells protect IL-2 receptor α-deficient mice from systemic infection with herpes simplex virus type 2

IL-2R alpha-defcient (IL-2R alpha(-/-)) mice exhibit an impaired activation-induced cell death for T cells and develop abnormal T cell activation with age. In our study, we found that IL-2R alpha(-/-) mice at the age of 5 wk contained an increased number of CD44(+)CD69(-)CD8(+) T cells in lymph nodes, which expressed a high intensity of IL-2R beta and vigorously proliferated in response to a high dose of IL-15 or IL-2, The T cells produced a large amount of IFN-gamma in response to IL-15 plus IL-li in a TCR-independent bystander manner. When IL-2R alpha(-/-) mice were inoculated i.p. with HSV type 2 (HSV-2) 186 strain, they showed resistance to the infection accompanied by an increased level of serum IL-15, The depletion of CD8(+) T cells by in vivo administration of anti-CD8 mAb rendered IL-2R alpha(-/-) mice susceptible to HSV-2-induced lethality, These results suggest that memory-type CD8(+) T cells play a novel role in the protection against HSV-2 infection in IL-2R alpha(-/-) mice.