Abstract

Memory T cells are critical to protect us from recurring infections. Their instantaneous reactivity to pathogens is empowered by persistent expression of cytokine mRNA. How aberrant cytokine production of this pre-formed mRNA is prevented in the absence of infection remains, however, unresolved. Here, I will discuss how post-transcriptional regulation through AU-rich elements is key to block chronic production of cytokines in memory T cells. Importantly, for swift recall responses to infection, this translational block must be rapidly relieved and pre-formed cytokine mRNA serves as ready-to-be-translated template. This switch is achieved by loss of the suppressive capacity of the RNA -binding protein ZFP36L2 . Finally, I propose that altering the post-transcriptional regulation of IFN production can be exploited to improve the efficacy of T cell therapy for cancer treatment.