We have explored the interactions between the NFκB and Cdk-Rb-E2F pathways in controlling T cell fate following antigen stimulation. The inhibition of NFκB in antigen-stimulated T cells results in apoptosis but does not inhibit E2F activation and S phase entry. IκB-induced apoptosis coincides with the superinduction of p73 expression and activity. G1 Cdk activity is required for IκB-induced apoptosis and the induction of p73. Importantly, p73 deficiency rescues activated T cells from the apoptosis resulting from the inhibition of NFκB. Thus, Cdk2 activation sends signals for both cell cycle progression and apoptosis, the latter of which must be blocked by NFκB to allow for proliferation.
Wan, Y. Y., & DeGregori, J. (2003). The survival of antigen-stimulated T cells requires NFκB-mediated inhibition of p73 expression. Immunity, 18(3), 331–342. https://doi.org/10.1016/S1074-7613(03)00053-0