CRISPR screening reveals targets to reprogram long-lived effector CD8+ T cells for cancer therapy [microarray]

CD8+ T cells can be reprogrammed for better persistence and robust effector function in TME. By performing an in vivo pooled CRISPR-Cas9 mutagenesis screening of metabolism-associated factors, we identify Regnase-1 as a major negative regulator of antitumor responses, whose deficiency results in drastically increased CD8+ T cell accumulation in tumors We used microarrays to compare the global transcription profiles of Regnase1-null, Ptpn2/Regnase1-null and Socs1/Regnase1-null tumor infiltrating CD8+ T cell populations In total 24 samples were analyzed: TIL CD8+ cells (Regnase1-null, n = 12; Ptpn2/Regnase1-null, n=4;Socs1/Regnase1-null, n = 4).