The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/4/1315/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 8, April 19, 1999 1315-1328

Articles

Two Roads Diverged: Interferon {alpha}/β– and Interleukin 12–mediated Pathways in Promoting T Cell Interferon {gamma} Responses during Viral Infection

Leslie P. Cousens*, Ron Peterson{ddagger}, Sang Hsu{ddagger}, Andrew Dorner{ddagger}, John D. Altman§, Rafi Ahmed§, and Christine A. Biron*

From the * Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912; the {ddagger} 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

Viral infections induce CD8 T cell expansion and interferon (IFN)-{gamma} 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-{gamma} has not been detected during viral infections. Moreover, certain viruses fail to induce IL-12, and elicit high levels of IFN-{alpha}/β to negatively regulate it. The endogenous factors promoting virus-induced T cell IFN-{gamma} 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-{gamma} response was dependent on endogenous IFN-{alpha}/β effects, but was IL-12 independent. In contrast, in the absence of IFN-{alpha}/β functions, an IL-12 response was revealed and substituted an alternative pathway to IFN-{gamma}. IFN-{alpha}/β–mediated effects resulted in enhanced, but the alternative pathway also promoted, resistance to infection. These observations define uniquely important IFN-{alpha}/β–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.

Key Words: T cell • virus • interferon {alpha}/β • interleukin 12 • interferon {gamma}

Address correspondence to Christine A. Biron, Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Box G-B629, Brown University, Providence, RI 02912. Phone: 401-863-2921; Fax: 401-863-9045; E-mail: christine_biron{at}brown.edu

Abbreviations used: CM, conditioned media; LCMV, lymphocytic choriomeningitis virus; MCMV, murine cytomegalovirus; WT, wild-type.


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