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-Deficient Mice from Systemic Infection with Herpes Simplex Virus Type 21
Laboratories of
*
Host Defense and Germfree Life and
Virology, Research Institute of Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan
IL-2R
-deficient (IL-2R-/-) 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-/- 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-2Rß
and vigorously proliferated in response to a high dose of IL-15 or
IL-2. The T cells produced a large amount of IFN-
in response to
IL-15 plus IL-12 in a TCR-independent bystander manner. When
IL-2R-/- 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-/- 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-/- mice.
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