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Eph/ephrinB signalling is involved in the survival of thymic epithelial cells
Author(s) -
GarcíaCeca Javier,
Alfaro David,
MonteroHerradón Sara,
Zapata Agustín G
Publication year - 2013
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2012.59
Subject(s) - erythropoietin producing hepatocellular (eph) receptor , tec , ephrin , microbiology and biotechnology , embryonic stem cell , biology , apoptosis , in vitro , in vivo , receptor tyrosine kinase , thymocyte , cancer research , signal transduction , immunology , antigen , biochemistry , cd8 , genetics , ionosphere , physics , astronomy , gene
The signals that determine the survival/death of the thymic epithelial cells (TECs) component during embryonic development of the thymus are largely unknown. In this study, we combine different in vivo and in vitro experimental approaches to define the role played by the tyrosine kinase receptors EphB2 and EphB3 and their ligands, ephrinsB, in the survival of embryonic and newborn (NB) TECs. Our results conclude that EphB2 and EphB3 are involved in the control of TEC survival and that the absence of these molecules causes increased apoptotic TEC proportions that result in decreased numbers of thymic cells and a smaller‐sized gland. Furthermore, in vitro studies using either EphB2‐Fc or ephrinB1‐Fc fusion proteins demonstrate that the blockade of Eph/ephrinB signalling increases TEC apoptosis, whereas its activation rescues TECs from cell death. In these assays, both heterotypic thymocyte–TEC and homotypic TEC–TEC interactions are important for Eph/ephrinB‐mediated TEC survival.