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PLoS One ; 10(9): e0138835, 2015.
Article in English | MEDLINE | ID: mdl-26407069

ABSTRACT

The Eph receptor tyrosine kinases interact with their ephrin ligands on adjacent cells to facilitate contact-dependent cell communication. Ephrin B ligands are expressed on T cells and have been suggested to act as co-stimulatory molecules during T cell activation. There are no detailed reports of the expression and modulation of EphB receptors on dendritic cells, the main antigen presenting cells that interact with T cells. Here we show that mouse splenic dendritic cells (DC) and bone-marrow derived DCs (BMDC) express EphB2, a member of the EphB family. EphB2 expression is modulated by ligation of TLR4 and TLR9 and also by interaction with ephrin B ligands. Co-localization of EphB2 with MHC-II is also consistent with a potential role in T cell activation. However, BMDCs derived from EphB2 deficient mice were able to present antigen in the context of MHC-II and produce T cell activating cytokines to the same extent as intact DCs. Collectively our data suggest that EphB2 may contribute to DC responses, but that EphB2 is not required for T cell activation. This result may have arisen because DCs express other members of the EphB receptor family, EphB3, EphB4 and EphB6, all of which can interact with ephrin B ligands, or because EphB2 may be playing a role in another aspect of DC biology such as migration.


Subject(s)
Dendritic Cells/immunology , Dendritic Cells/metabolism , Gene Expression Regulation , Lymphocyte Activation/immunology , Receptor, EphB2/genetics , T-Lymphocytes/immunology , Toll-Like Receptors/metabolism , Animals , CD4-Positive T-Lymphocytes/immunology , CD4-Positive T-Lymphocytes/metabolism , Cell Line , Cytokines/biosynthesis , Female , Histocompatibility Antigens Class II/immunology , Histocompatibility Antigens Class II/metabolism , Humans , Inflammation Mediators/metabolism , Ligands , Lymphocyte Activation/genetics , Mice , Mice, Knockout , Protein Binding , Receptor, EphB2/deficiency , Receptor, EphB2/metabolism , T-Lymphocytes/metabolism
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