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* Department of Medical Microbiology and Immunology, University of Ulm, Ulm, Germany;
Institute of Hepatology, University College of London, London, United Kingdom; and
German Research Centre for Biotechnology, Braunschweig, Germany
Pleiotropic, immunomodulatory effects of type I IFN on T cell responses are emerging. We used vaccine-induced, antiviral CD8+ T cell responses in IFN-
(IFN-–/–)- or type I IFN receptor (IFNAR–/–)-deficient mice to study immunomodulating effects of type I IFN that are not complicated by the interference of a concomitant virus infection. Compared with normal B6 mice, IFNAR–/– or IFN-–/– mice have normal numbers of CD4+ and CD8+ T cells, and CD25+FoxP3+ T regulatory (TR) cells in liver and spleen. Twice as many CD8+ T cells specific for different class I-restricted epitopes develop in IFNAR–/– or IFN-–/– mice than in normal animals after peptide- or DNA-based vaccination. IFN-
and TNF-
production and clonal expansion of specific CD8+ T cells from normal and knockout mice are similar. CD25+FoxP3+ TR cells down-modulate vaccine-primed CD8+ T cell responses in normal, IFNAR–/–, or IFN-–/– mice to a comparable extent. Low IFN- or IFN- doses (500–103 U/mouse) down-modulate CD8+ T cells priming in vivo. IFNAR- and IFN--deficient mice generate 2- to 3-fold lower numbers of IL-10-producing CD4+ T cells after polyclonal or specific stimulation in vitro or in vivo. CD8+ T cell responses are thus subjected to negative control by both CD25+FoxP3+ TR cells and CD4+IL-10+ TR1 cells, but only development of the latter TR cells depends on type I IFN.
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