Fig. 6: TIGIT.synNotch.aCD73-iNK cells demonstrate enhanced infiltration and reduced exhaustion over single-target controls.
From: synNotch-programmed iPSC-derived NK cells usurp TIGIT and CD73 activities for glioblastoma therapy
A–H Representative IHC staining (200 x magnification) of GzB, NKp46, CD73, and CD155 in whole brain sections harvested from intracranial tumor-bearing mice treated with PBS, WT iNK or synNotch-engineered iNK cells, and quantification/scoring of IHC staining; GzB Granzyme B (n = 4 intratumoral sections; ordinary one-way ANOVA, Tukey’s multiple comparison test). I Tumor weight of GBM43 WT flank tumors harvested from iNK or PBS-treated mice (n = 4 mice/group; ordinary one-way ANOVA, Tukey’s multiple comparison test) (Supplementary Fig. 17). J Quantification of NK cell infiltration in GBM43 WT flank tumors (n = 4 mice/group; ordinary one-way ANOVA, Tukey’s multiple comparison test) (Supplementary Fig. 17). K Fold MFI and L percentage of NK receptor expression measured on iNK cells harvested from treated GBM43 WT flank tumors (n = 3 mice/group; two-way ANOVA, Tukey’s multiple comparison test, simple row effects) (Supplementary Fig. 17). Data are presented as mean values +/- SEM. Source data are provided as a Source Data file.
