Antitumor T-Cell Function Requires CPEB4-Mediated Adaptation to Chronic Endoplasmic Reticulum Stress

Researchers found that, in effector CD8 T lymphocytes, RNA-binding protein CPEB4 constituted a new branch of the unfolded protein response (UPR) that allowed cells to adapt to sustained endoplasmic reticulum stress, yet remained decoupled from the terminal UPR.