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*Substance via MeSH
The Journal of Immunology, 2006, 176: 4682-4689.
Copyright © 2006 by The American Association of Immunologists

Direct Stimulation of T Cells by Type I IFN Enhances the CD8+ T Cell Response during Cross-Priming1

Agnes Le Bon*, Vanessa Durand*, Elisabeth Kamphuis{dagger}, Clare Thompson*, Silvia Bulfone-Paus{ddagger}, Cornelia Rossmann*, Ulrich Kalinke{dagger} and David F. Tough2,*

* The Edward Jenner Institute for Vaccine Research, Compton, United Kingdom; {dagger} Department of Immunology, Paul Ehrlich Institute, Langen, Germany; and {ddagger} Department of Immunology and Cell Biology, Research Center Borstel, Borstel, Germany

Type I IFN (IFN-{alpha}beta), 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-{alpha}beta induces cross-priming, comparing CD8+ T cell responses generated against soluble protein Ags in the presence or absence of IFN-{alpha}beta. Injection of IFN-{alpha} 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-{alpha}-induced cross-priming. Conversely, expression of the IFN-{alpha}betaR by T cells was shown to be necessary for effective stimulation of the response by IFN-{alpha}. The finding that T cells represent direct targets of IFN-{alpha}beta-mediated stimulation reveals an additional mechanism by which the innate response to infection promotes adaptive immunity.




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