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CD40 Ligand and CTLA-4 Are Reciprocally Regulated in the Th1 Cell Proliferative Response Sustained by CD8⁺ Dendritic Cells¹

Department of Experimental Medicine, University of Perugia, Perugia, Italy

Subsets of murine dendritic cells (DCs) from the spleen differ in their ability to induce proliferative responses in both primary and secondary CD4⁺ T cells. Recent evidence indicates that lymphoid-related CD8⁺ DCs fail to provide appropriate signals to freshly isolated secondary CD4⁺ T cells to sustain their proliferation in vitro. In the present study, we examined peptide-pulsed CD8^- and CD8⁺ DCs for ability to stimulate Th1 and Th2 cell clones with the same Ag specificity. Defective ability to induce proliferation was selectively shown by CD8⁺ DCs presenting Ag to the Th1 clone. The deficiency in CD8⁺ DCs was overcome by CD40 triggering before peptide pulsing. When exposed to CD8⁺ DCs in the absence of CD40 activation, the Th1 clone expressed low levels of CD40 ligand and high levels of surface CTLA-4. Neutralization of CTLA-4 during the DC/T cell coculture resulted in increased CD40 ligand expression and proliferation of T cells. Remarkably, the activation of CD40 on DCs under conditions that would increase Th1 cell proliferation, also resulted in down-regulation of surface CTLA-4. These results confirm differential effects of CD8⁺ and CD8^- DCs in the stimulation of Ag-primed Th cells. In addition, they suggest that reciprocal regulation of CD40 ligand and CTLA-4 expression occurs in Th1 cells exposed to CD8⁺ DCs.

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