Notch promotes survival of pre-T cells at the beta-selection checkpoint by regulating cellular metabolism.

摘要: Notch signals are necessary for the functional outcomes of T cell receptor beta-selection, including differentiation, proliferation and rescue from apoptosis. The mechanism underlying this requirement development is unknown. Here we show that Delta-like 1 ligand interactions promoted survival CD4(-)CD8(-) pre-T cells through maintenance size, glucose uptake metabolism. Furthermore, trophic effects signaling were mediated by pathway phosphatidylinositol-3-OH kinase Akt, such expression active Atk overcame in beta-selection. Collectively, our results demonstrate involvement receptor-ligand regulation cellular metabolism, thus enabling autonomous capacity complex.