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* Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912; and
Department of Microbiology, Ohio State University, Columbus, OH 43210
The kinetics of CD8 T cell IFN-
responses as they occur in situ
are defined here during lymphocytic choriomeningitis virus (LCMV)
infections, and a unique mechanism for the innate cytokines IFN-
and IL-18 in promoting these responses is defined. Infections of mice
with Armstrong or WE strains of LCMV induced an unexpectedly early day
4 IFN- response detectable in serum samples and spleen and liver
homogenates. Production of IFN- was MHC class I/CD8 dependent, but
did not require IL-12, NK cells, TCR-
T cells, MHC class II, or
CD4 T cells. Peak response required specific Ag recognition, as
administration of antagonist peptide partially impaired day 4 IFN-
induction, and viral peptide stimulation enhanced CD8 T cell IFN-
expression in culture. The IFN- response was associated with IL-18
and IFN- expression. Furthermore, both factors augmented
peptide-driven IFN- production in culture, and mice lacking IL-18 or
IFN- functions had reduced day 4 IFN-. Collectively, these
results demonstrate that during viral infections, there is a dramatic
in vivo CD8 T cell response preceding maximal expansion of these cells,
and that the mechanism supporting this response is dependent on
endogenous innate cytokines. Because stimulation by microbial products
is linked to innate cytokine expression, the studies also suggest a
pathway for precisely limiting T cell functions to times of
need.
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