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. 2020 Dec 15;53(6):1215–1229.e8. doi: 10.1016/j.immuni.2020.10.020

Figure 1.

Figure 1

Ablation of Cancer Cell-Intrinsic COX Alters the Intratumoral Accumulation of Select Innate Immune Cell Subsets

(A) Kaplan-Meier plots showing the fraction of tumor-bearing wild-type (n = 10), Tmem173−/− (n = 5), Cgas−/− (n = 5), Trif−/− (n = 7), Mavs−/− (n = 6), and Myd88−/− (n = 6) mice injected with Ptgs−/− or Ptgs+/+ melanoma tumor cells in wild-type (n = 10) hosts.

(B–D) Immune cell infiltrate analysis of Ptgs+/+, Ptgs−/−, and Ptgs−/−+COX-2 tumors 4 days post-implantation. (B) Two-dimensional distributed stochastic neighbor embedding (t-SNE) projections of CD45+ cells for each group (n = 6 concatenated samples per group). The frequency and the number of intratumoral neutrophils (C) and NK cells (D) are shown.

(E) Weight of Ptgs+/+ and Ptgs−/− tumors 4 days post-implantation in wild-type, NK cell-depleted, or Rag1−/− mice.

(F) Ptgs+/+, Ptgs−/− (+/− synthetic PGE2), and Ptgs−/−+COX-2 melanoma cells tested for susceptibility to NK cell-mediated killing. E:T refers to ratio of effector:target cells.

(G) Percentage of NK cells contacting either 1 or more (2–5) Ptgs+/+, Ptgs−/−, or Ptgs−/−+COX2 targets.

(H) Violin plots representing the number of interactions and the cumulative contact time of NK cells with Ptgs+/+, Ptgs−/−, and Ptgs−/−+COX-2 targets. Data are expressed as mean ± SEM, one-way ANOVA (C–F and H) or Fisher’s exact test. (G).