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. 2024 Feb 19;30(9):1934–1944. doi: 10.1158/1078-0432.CCR-23-3477

Figure 1.

Figure 1. aPD1-resistant model shows reduced priming due to cDC1 dysfunction in tumor-draining lymph nodes (DLN). A, In vivo tumor growth of MOC1P-ova after treatment with aPD1 (250 μg IP on days 3, 6, and 9) or FTY720 (10 μg IP daily from one day before inoculation). (n = 4 tumors for each group). B and C, Flow-cytometric analysis of MOC1P-ova/MOC1esc1-ova DLN on day 10 after inoculation (n = 4 for each group, representative data of two independent experiments). D, Representation of experiment in E. E, Tumor DLN from orthotopically inoculated MOC1P-ova/esc1-ova–bearing mice were harvested on day 10 and stimulated with SIINFEKL peptide for 48 hours to assess IFNγ production by ELISA (n = 4 for each group, representative data of two independent experiments). F, Flow-cytometric analysis of costimulatory markers on Xcr1+ DC in DLN of MOC1P-ova/MOC1esc1-ova harvested 10 days after tumor inoculation (n = 4 for each group, representative data of two independent experiments). G, Representation of experiment in H. H, Xcr1+ DC magnetically isolated from DLN of MOC1P-ova/MOC1esc1-ova were cocultured with CD8+ OT1 T cells to test priming ability evaluated by IFNγ ELISA (n = 5–6, representative data of two independent experiments). Data are plotted as mean ± SEM in A and individual data with mean ± SD in all other panels. Data were analyzed using two-way ANOVA with multiple comparison for A and Mann–Whitney U test to generate two-tailed P values in B, C, E, F, and H. (D and G were generated by using BioRender under granted license.) *, P < 0.05; **, P < 0.01; ns, not significant.

aPD1-resistant model shows reduced priming due to cDC1 dysfunction in tumor-draining lymph nodes (DLN). A,In vivo tumor growth of MOC1P-ova after treatment with aPD1 (250 μg IP on days 3, 6, and 9) or FTY720 (10 μg IP daily from one day before inoculation). (n = 4 tumors for each group). B and C, Flow-cytometric analysis of MOC1P-ova/MOC1esc1-ova DLN on day 10 after inoculation (n = 4 for each group, representative data of two independent experiments). D, Representation of experiment in E. E, Tumor DLN from orthotopically inoculated MOC1P-ova/esc1-ova–bearing mice were harvested on day 10 and stimulated with SIINFEKL peptide for 48 hours to assess IFNγ production by ELISA (n = 4 for each group, representative data of two independent experiments). F, Flow-cytometric analysis of costimulatory markers on Xcr1+ DC in DLN of MOC1P-ova/MOC1esc1-ova harvested 10 days after tumor inoculation (n = 4 for each group, representative data of two independent experiments). G, Representation of experiment in H. H, Xcr1+ DC magnetically isolated from DLN of MOC1P-ova/MOC1esc1-ova were cocultured with CD8+ OT1 T cells to test priming ability evaluated by IFNγ ELISA (n = 5–6, representative data of two independent experiments). Data are plotted as mean ± SEM in A and individual data with mean ± SD in all other panels. Data were analyzed using two-way ANOVA with multiple comparison for A and Mann–Whitney U test to generate two-tailed P values in B, C, E, F, and H. (D and G were generated by using BioRender under granted license.) *, P < 0.05; **, P < 0.01; ns, not significant.