NAC1 constrains CD4 +T cell memory formation through the ROCK1-mediated pathway

Abstract Nucleus accumbens-associated protein 1 (NAC1) is a transcriptional co-factor that has been extensively investigated in cancer biology. Our recent studies indicate NAC1 can modulate the functional activity of regulatory T cells and tumoral expression restrains antitumor immunity. However, little known about its regulation memory cells. In current study, we analyzed CD4 +T from wild type (WT) NAC1-decificient (−/−) mice used vaccinia virus (VACV) as tool to investigate precise role mechanism controlling cell memory. vitro, identified essential for metabolism, including both glycolysis oxidative phosphorylation, which positively modulates survival. We also revealed deficiency an interruption AMPK-mTOR pathway, resulting decreased defective autophagy Mechanically, loss downregulates ROCK1 reduces phosphorylation stabilization BECLIN1. When overexpressing −/−CD4 cells, interrupted pathway were restored. vivo, when i.p.challenged with VACV, −/−mice had improved VACV-specific +memory formation at 35 days compared WT mice. Furthermore, adoptively transferred experiments (Thy1.2 +) congenic hosts (Thy1.1 +), increased was reverted normal level. Conclusively, define acts suppressor through ROCK1-mediated targeting may be adapted promote development.