Figure 8.
STING antitumor immune responses in CXCR3-deficient mice. (A) Schematic treatment schedule for C57BL/6 (wild-type [WT]) or CXCR3-/- mice engrafted subcutaneously with KPC1242 PDA cells. (B) mRNA expression of CXCR3 in murine KPC cell lines, WT mouse spleen, or CD3/CD28-activated WT T cells. NRAMP non-coding region was amplified as a control for genomic DNA. +, WT mouse positive control. (C) Expression of CXCR3 and CD69 early activation marker on T cells derived from spleens of CXCR3-/- or WT mice measured by flow cytometry at 24 and 48 hours after activation. (D) Tumor volume from WT (black bars) and CXCR3-/- (blue bars) mice treated intratumorally with 450 μg DMXAA or vehicle control. (E and F) Cellular frequencies of tumor-infiltrating pan-leukocyte CD45+ immune cells (E) and tumor-infiltrating CD8+ cytolytic T cells (F). (G) Frequencies of CD3+ or CD8+ cells within spleens of PDA tumor-bearing WT or CXCR3-/- mice. (H and I) Within spleens of non–tumor-bearing WT or CXCR3-/- mice, an analysis of CD3+ T cell frequencies (H) and additional cell-type frequencies and phenotypes (I). (J) Expression of CCR5, another surface chemokine on activated splenocytes, remains consistent between WT and CXCR3-/- mice. Error bars represent mean ± SEM. n = 4–8 mice from 2 independent experiments. ns, not significant. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001.