IL-2Rα-deficient (IL-2Rα(-/-)) 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-2Rα(-/-) 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-2Rβ and vigorously proliferated in response to a high dose of IL-15 or IL-2. The T cells produced a large amount of IFN-γ in response to IL-15 plus IL-12 in a TCR-independent bystander manner. When IL-2Rα(-/-) 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-I5. The depletion of CD8+ T cells by in vivo administration of anti-CD8 mAb rendered IL-2Rα(-/-) 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-2Rα(-/-) mice.
All Science Journal Classification (ASJC) codes
- Immunology and Allergy