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1
*
Department of Microbiology and
Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242
Single Ag-specific CD8+ T cells from IFN-
-deficient
(GKO) or perforin-deficient (PKO) mice provide substantial immunity
against murine infection with Listeria monocytogenes. To
address the potential for redundancy between perforin and IFN- as
CD8+ T cell effector mechanisms, we generated
perforin/IFN- (PKO/GKO) double-deficient mice. PKO/GKO-derived
CD8+ T cells specific for the immunodominant listeriolysin
O (LLO91–99) epitope provide immunity to LM infection
similar to that provided by Ag-matched wild-type (WT) CD8+
T cells in the liver but reduced in the spleen. Strikingly, polyclonal
CD8+ T cells from immunized PKO/GKO mice were 
100-fold
more potent in reducing bacterial numbers than the same number of
polyclonal CD8+ T cells from immunized WT mice. This result
is probably quantitative, because the frequency of the CD8+
T cell response against the immunodominant LLO91–99
epitope is >4.5-fold higher in PKO/GKO mice than WT mice at 7 days
after identical immunizations. Moreover, PKO/GKO mice can be immunized
by a single infection with attenuated Listeria to resist
>80,000-fold higher challenges with virulent organisms than naive
PKO/GKO mice. These data demonstrate that neither perforin nor IFN-
is required for the development or expression of adaptive immunity to
LM. In addition, the results suggest the potential for perforin and
IFN- to regulate the magnitude of the CD8+ T cell
response to infection.
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