Figure 5.
Recruitment of cDC1 into Tumors by XCL1 and CCL5 Promotes Tumor Immune Control
(A) Migration of cDC1 toward CCL5 or XCL1.
(B) cDC1 accumulation in Ptgs1/Ptgs2−/− BRAFV600E tumors in WT mice injected with anti-CCL5 and anti-XCL1 antibodies or the respective isotype-matched controls.
(C) Quantification of intratumoral cDC1 4 days after s.c. injection of 2 × 106Ptgs1/Ptgs2−/− BRAFV600E cells expressing CCL5 or XCL1 or transduced with an empty vector (EMPTY).
(D and E) Growth of the tumors in (C) after s.c. transplantation of 2 × 105 cells into (D) WT or (E) Batf3−/− mice.
(F) Growth of 2 × 105 EMPTY or XCL1-expressing Ptgs1/Ptgs2−/− BRAFV600E cells in WT mice with or without NK cell depletion after s.c. transplantation.
(G) Quantification of intratumoral cDC1 4 days after s.c. injection of 2 × 106 B16-OVA cells EMPTY or overexpressing CCL5 or XCL1 into WT mice.
(H) Tumor growth following s.c. injection of 2 × 105 B16-OVA cells EMPTY or overexpressing CCL5 or XCL1.
(I and J) Same as (G) and (H) but using Ptgs2−/− CT26 colorectal cancer cells.
Data in (A) are from one of three independent experiments and are shown as mean of duplicate transwells ±SD. Pooled data from at least two experiments are shown in (B)–(J) and represented as mean of each group of mice ± SEM; (B–J): n.s., non-significant, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
See also Figure S5.