Extended Data Fig. 1: LMP1+ B cells drive CD4+ T cell differentiation into EOMES-programed granzyme/perforin-dependent cytotoxic effectors.
From: Mechanism of EBV inducing anti-tumour immunity and its therapeutic use
a, FACS analysis of EOMES, granzyme B and perforin expression in CD4 cells, from mice with CD4-specific Eomes knockout (Cd4-cre;EomesF/F) or with normal levels of EOMES (Cd4-cre), primed in vitro by LMP1+ B cells. Granzyme B and perforin levels in EOMES+ CD4 cells from Cd4-cre mice (P3) were compared with those in EOMES– CD4 cells from the same mice (P2) or Cd4-cre;EomesF/F mice (P1), and are shown on the right. For these analyses, FOXP3+ Treg cells were excluded. b, c, Killing activity of EOMES-null CD4 cells (from Cd4-cre;EomesF/F mice) or perforin-null CD4 cells (from Prf1–/– mice) in comparison with wide-type (WT) CD4 cells, primed as in a, against LMP1+ lymphoma cell targets. E:T ratio, effector-to-target cell ratio. All mice are on the B6 background. Statistics and reproducibility are presented in the Supplementary Information.
