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. 2022 Mar 14;10(3):e004129. doi: 10.1136/jitc-2021-004129

Figure 8.

Figure 8

ATP11B depletion activates anti-pancreatic cancer immunity. (A–F) Inhibition of pancreatic tumor growth by ATP11B depletion in an immune system-dependent manner. (A–B) WT and ATP11B KO KPC cells separately orthotopically inoculated into the immunodeficient and immunocompetent mice. Survival curves of immunodeficient (A) and immunocompetent mice (B). WT and ATP11B KO KPC cells were separately orthotopically inoculated into the immunodeficient and immunocompetent mice (n=6). Representative images and weight of tumors in the immunodeficient (C) and immunocompetent mice (D) were individually recorded at the experimental endpoints. Representative FACS images of tumor-infiltrating lymphocytes in immunocompetent mice were shown and further quantified (E–F). (G) Representative images of PD-L1 immunohistochemical staining shown and further quantified. (H–L) Abolition of the therapeutic efficacy of LTX-315 in pancreatic cancer by ATP11B KO. WT and ATP11B KO KPC cells subcutaneous inoculated into the immunocompetent mice (n=5) treated with LTX-315. Growth curves of tumors were recorded at the indicated time points (H). Representative images of tumor weight (I) and tumors (J) were individually recorded at the experimental endpoints. Representative images of FACS analysis of T cell infiltration (K) and T cell function (L) were individually shown and further quantified. Results are presented as mean±SD from one representative experiment. *p<0.05, **p<0.01, ***p<0.001 by a two-tailed t-test; KO, knockout; NS, not significant; PD-L1, programmed cell death ligand 1; WT, wild type.