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J. Exp. Med.,
Volume 189, Number 8, April 19, 1999 1315-1328
/
- and Interleukin
12-mediated Pathways in Promoting T Cell Interferon 
Responses during Viral Infection
By
From the * Department of Molecular Microbiology and Immunology, Division of Biology and Medicine,
Brown University, Providence, Rhode Island 02912; the Viral infections induce CD8 T cell expansion and interferon (IFN)- Genetics Institute, Inc., Andover,
Massachusetts 01810; and the § Emory Vaccine Center and Department of Microbiology and
Immunology, Emory University School of Medicine, Atlanta, Georgia 30322
production for defense,
but the innate cytokines shaping these responses have not been identified. Although interleukin (IL)-12 has the potential to contribute, IL-12-dependent T cell IFN- has not been detected
during viral infections. Moreover, certain viruses fail to induce IL-12, and elicit high levels of IFN-
/
to negatively regulate it. The endogenous factors promoting virus-induced T cell
IFN- production were defined in studies evaluating CD8 T cell responses during lymphocytic
choriomeningitis virus infections of mice. Two divergent supporting pathways were characterized. Under normal conditions of infections, the CD8 T cell IFN- response was dependent
on endogenous IFN-/ effects, but was IL-12 independent. In contrast, in the absence of
IFN-/ functions, an IL-12 response was revealed and substituted an alternative pathway to
IFN-. IFN-/-mediated effects resulted in enhanced, but the alternative pathway also promoted, resistance to infection. These observations define uniquely important IFN-/-controlled pathways shaping T cell responses during viral infections, and demonstrate plasticity of
immune responses in accessing divergent innate mechanisms to achieve similar ultimate goals.
/;
interleukin 12;
interferon
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