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Two critical functions of dendritic cells (DC) are to activate and functionally polarize T cells. Activated T cells can, in turn, influence DC maturation, although their effect on  de novo  DC development is poorly understood. Here we report that activation of T cells in mice, with either an anti-CD3 antibody or super antigen, drives the rapid formation of CD209 + CD11b + CD11c +  MHC II +  DC from monocytic precursors (Mo-DC). GM-CSF is produced by T cells following activation, but surprisingly, it is not required for the formation of CD209 +  Mo-DC. CD40L, however, is critical for the full induction of Mo-DC following T cell activation. T cell induced CD209 +  Mo-DC are comparable to conventional CD209 -  DC in their ability to stimulate T cell proliferation. However, in contrast to conventional CD209 -  DC, CD209 +  Mo-DC fail to effectively polarize T cells, as indicated by a paucity of T cell cytokine production. The inability of CD209 +  Mo-DC to polarize T cells is partly explained by increased expression of PDL-2, since blockade of this molecule restores some polarizing capacity to the Mo-DC. These findings expand the range of signals capable of driving Mo-DC differentiation  in vivo  beyond exogenous microbial factors to include endogenous factors produced following T cell activation.

In Vivo T Cell Activation Induces the Formation of CD209+ PDL-2+ Dendritic Cells