The observation that TCR engineering combined with Tet-regulated IL-12 expression can achieve tumor immunity without the side effects that are usually associated with the <i>in vivo</i> use of IL-12 warrants translation of this concept into the clinic.
Here, we identify the GTPase-activating protein (GAP) Rasal1 as a novel TCR-ZAP-70 binding protein that negatively regulates T-cell activation and tumor immunity.
In this review, we will summarize the role(s) of NOTCH signaling in T-cell anti-tumor immunity as well as TCR- and chimeric antigen receptor-based immunotherapies.
TCR-alpha/beta(+) cells were required to eliminate Panc02.MUC1 tumors, while TCR-gamma/delta(+) cells played a suppressive non-MUC1-specific role in anti-Panc02 tumor immunity.