A dataset on NFKB1/NFKB2 knockout Jurkat cells and primary CD4+ T cells generated by CRISPR/Cas9 mediated gene disruption.

Therefore, we genetically modified Jurkat leukemic cells using the clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 technology to better understand the NFKB signaling mechanisms. IKAROS family zinc finger-2 levels were downregulated in NFKB2-knocked-out cells but upregulated in NFKB1-knocked-out cells.

To further understand the biological roles of NFKB signaling in CD4+ T cells, NFKB1/NFKB2 loci of human primary CD4+ T cells were genetically edited using the CRISPR/CRISPR-associated protein 9 technology. Quantitative polymerase chain reaction and fluorescence-activated cell sorting revealed the similar phenotypes and gene expression profiles of NFKB1/NFKB2-knocked-out human CD4+ T cells.