The effect of conditional EFNB1 deletion in the T cell compartment on T cell development and function

The mice were of normal size and cellularity in the thymus and spleen and had normal T cell subpopulations in these organs. The bone marrow progenitors from KO mice and WT control mice repopulated host spleen T cell pool to similar extents. The activation and proliferation of KO T cells was comparable to that of control mice. Na？ve KO CD4 cells showed an ability to differentiate into Th1, Th2, Th17 and Treg cells similar to control CD4 cells.Our results suggest that the function of EFNB1 in the T cell compartment could be compensated by other members of the EFN family, and that such redundancy safeguards the pivotal roles of EFNB1 in T cell development and function.Eph kinases are the largest family of cell surface receptor tyrosine kinases and can be divided into A and B subfamilies according to their sequence homology. The ligands of Ephs, ephrins (EFNs), are also cell surface molecules. EFNs are divided into A and B subfamilies. EFNAs are GPI-anchored cell surface proteins and EFNBs are transmembrane cell surface proteins. Ephs and EFNs interact promiscuously. EphA members mainly interact with EFNA members, while EphB members mainly interact with EFNB members. When Ephs and EFNs interact, signals are transmitted in both directions, i.e., from Ephs to EFNs and from EFNs to Ephs. Such bi-directional signalling is called forward and reversed signalling respectively [1].EFNB1 is involved in the development and function of the central nervous system [2]. It is also essential in bone maintenance and remodelling [3]. EFNB1 expression in platelets contributes to the clotting process [4]. Its expression on kidney epithelial cells (podocytes) likely plays a role in glomerular filtration [5]. EFNB1 is involved in intestinal epithelial cell homeostasis [6]. We have shown that EFNB1 forward signalling through their Eph receptors can costimulate peripheral T cells in terms of enhancing cytokine production and proliferation in vitro and enhance thymocyte survival [7,8]. To furt