Expression of the Receptor Tyrosine Kinase EphB2 on Dendritic Cells Is Modulated by Toll-Like Receptor Ligation but Is Not Required for T Cell Activation
| Autor: | Tracey J. Lamb, Patrice N. Mimche, David S. J. Fenne, Lauren E. Hudson, Shirley Keeton, Thayer King, Kendra M. Quicke, Lauren M. Brady |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
CD4-Positive T-Lymphocytes
Receptor EphB2 T cell T-Lymphocytes lcsh:Medicine Biology Ligands Lymphocyte Activation EPH receptor B2 Cell Line 03 medical and health sciences Mice 0302 clinical medicine medicine Cytotoxic T cell Ephrin Animals Humans Antigen-presenting cell lcsh:Science 030304 developmental biology Mice Knockout 0303 health sciences Multidisciplinary ZAP70 Toll-Like Receptors lcsh:R Erythropoietin-producing hepatocellular (Eph) receptor Histocompatibility Antigens Class II CD28 Dendritic Cells Cell biology medicine.anatomical_structure Gene Expression Regulation Cytokines Female lcsh:Q Inflammation Mediators 030215 immunology Protein Binding Research Article |
| Zdroj: | PLoS ONE, Vol 10, Iss 9, p e0138835 (2015) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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