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Inhibits Presentation of a Tumor/Self Peptide by CD8
- Dendritic Cells Via Potentiation of the CD8+ Subset1
Department of Experimental Medicine, University of Perugia, Italy
Using an in vivo model of tumor/self peptide presentation for
induction of class I-restricted skin test reactivity, we have
previously shown that a minority population of CD8+
dendritic cells (DC) negatively regulates the induction of T cell
reactivity by peptide-loaded CD8- DC in DBA/2 mice.
However, the CD8- fraction can be primed by IL-12 to
overcome inhibition by the CD8+ subset when the two types
of DC are cotransferred into recipient hosts. We report here that
exposure of CD8+ DC to IFN-
greatly enhances their
inhibitory activity on Ag presentation by the other subset, blocking
the ability of IL-12-treated CD8- DC to overcome
suppression. In contrast, IFN- has no direct effects on the APC
function of the latter cells and does not interfere with IL-12
signaling. The negative regulatory effect triggered by IFN- in
CD8+ DC appears to involve interference with tryptophan
metabolism in vivo. Through tryptophan depletion affecting T cell
responses, IFN- acting on CD8+ DC may thus contribute to
regulation of immunity to tumor/self peptides presented by the
CD8- subset.
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