| First Author | Davidson MG | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 10 | Pages | e76258 |
| PubMed ID | 24098455 | Mgi Jnum | J:209037 |
| Mgi Id | MGI:5565575 | Doi | 10.1371/journal.pone.0076258 |
| Citation | Davidson MG, et al. (2013) In vivo T cell activation induces the formation of CD209(+) PDL-2(+) dendritic cells. PLoS One 8(10):e76258 |
| abstractText | 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. |
