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* The Edward Jenner Institute for Vaccine Research, Compton, United Kingdom;
Department of Immunology, Paul Ehrlich Institute, Langen, Germany; and
Department of Immunology and Cell Biology, Research Center Borstel, Borstel, Germany
Type I IFN (IFN-
), which is produced rapidly in response to infection, plays a key role in innate immunity and also acts as a stimulus for the adaptive immune response. We have investigated how IFN- induces cross-priming, comparing CD8+ T cell responses generated against soluble protein Ags in the presence or absence of IFN-. Injection of IFN- was found to prolong the proliferation and expansion of Ag-specific CD8+ T cells, which was associated with marked up-regulation of IL-2 and IL-15 receptors on Ag-specific cells and expression of IL-15 in the draining lymph node. Surprisingly, neither IL-2 nor IL-15 was required for IFN--induced cross-priming. Conversely, expression of the IFN-R by T cells was shown to be necessary for effective stimulation of the response by IFN-. The finding that T cells represent direct targets of IFN--mediated stimulation reveals an additional mechanism by which the innate response to infection promotes adaptive immunity.
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