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Production by CD4 T Cells, Whereas Neither Are Required for IFN- Production by CD8 T Cells after Listeria monocytogenes Infection
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,,,
* Department of Pediatrics,
Department of Immunology, and
Washington National Primate Center, University of Washington School of Medicine, Seattle, WA 98195
Differentiation of Ag-specific T cells into IFN-
producers is essential for protective immunity to intracellular pathogens. In addition to stimulation through the TCR and costimulatory molecules, IFN- production is thought to require other inflammatory cytokines. Two such inflammatory cytokines are IL-12 and type I IFN (IFN-I); both can play a role in priming naive T cells to produce IFN- in vitro. However, their role in priming Ag-specific T cells for IFN- production during experimental infection in vivo is less clear. In this study, we examine the requirements for IL-12 and IFN-I, either individually or in combination, for priming Ag-specific T cell IFN- production after Listeria monocytogenes (Lm) infection. Surprisingly, neither individual nor combined defects in IL-12 or IFN-I signaling altered IFN- production by Ag-specific CD8 T cells after Lm infection. In contrast, individual defects in either IL-12 or IFN-I signaling conferred partial (
50%) reductions, whereas combined deficiency in both IL-12 and IFN-I signaling conferred more dramatic (75–95%) reductions in IFN- production by Ag-specific CD4 T cells. The additive effects of IL-12 and IFN-I signaling on IFN- production by CD4 T cells were further demonstrated by adoptive transfer of transgenic IFN-IR+/+ and IFN-IR–/– CD4 T cells into normal and IL-12-deficient mice, and infection with rLm. These results demonstrate an important dichotomy between the signals required for priming IFN- production by CD4 and CD8 T cells in response to bacterial infection.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 Address correspondence and reprint requests to Dr. Sing Sing Way, 1959 Northeast Pacific Street, Box 357650, Seattle, WA 98195; E-mail address: singsing{at}u.washington.edu or Dr. Kaja Murali-Krishna, 1959 Northeast Pacific Street, Box 357650, Seattle, WA 98195; E-mail address: mkaja{at}u.washington.edu
2 S.S.W., C.H.-D., and G.A.K. contributed equally to this work.
3 Abbreviations used in this paper: LCMV, lymphocytic choriomeningitis virus; LLO, listeriolysin O; Lm, Listeria monocytogenes; WT, wild type.
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