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In Vivo T Cell Activation Induces the Formation of CD209+ PDL-2+ Dendritic Cells
Author(s) -
Matthew G. Davidson,
Michael N. Alonso,
Justin A. Kenkel,
Megan M. Suhoski,
Joseph C. González,
Robert Yuan,
Edgar G. Engleman
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0076258
Subject(s) - microbiology and biotechnology , t cell , chemistry , cd11c , dendritic cell , antigen presenting cell , mhc class ii , cd40 , biology , antigen , in vitro , cytotoxic t cell , immunology , immune system , biochemistry , phenotype , gene
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.

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