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Department of Experimental Medicine, University of Perugia, Perugia, Italy
The outcome of dendritic cell (DC) presentation of P815AB, a
tolerogenic tumor/self peptide, depends on a balance between the
respective immunogenic and tolerogenic properties of myeloid
(CD8
-) and lymphoid (CD8+) DC. We have
previously shown that CD8- DC can be primed by IL-12 to
overcome inhibition by the CD8+ subset and initiate
immunogenic presentation in vivo when the two types of peptide-pulsed
DC are cotransferred into recipient hosts. IFN-
enhances the
inhibitory activity of CD8+ DC on Ag presentation by the
other subset, blocking the ability of IL-12-treated CD8-
DC to overcome suppression. We report here that CD40 ligation on
lymphoid DC ablated their inhibitory function on Ag presentation as
well as IFN- potentiation of the effect. CD40 modulation of IFN-
action on lymphoid DC involved a reduction in IFN-R expression and
tryptophan-degrading ability. This effect was accompanied in vitro by
an impaired capacity of the CD40-modulated and IFN--treated DC to
initiate T cell apoptosis. In vivo, not only did CD40 triggering on
lymphoid DC abrogate their tolerogenic activity, but it also induced
the potential for immunogenic presentation of P815AB. Importantly, a
pattern similar to P815AB as well as CD40 modulation of lymphoid DC
function were observed on testing reactivity to NRP, a synthetic
peptide mimotope recognized by diabetogenic CD8+ T cells in
nonobese diabetic mice.
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