Function of CXCR3 in tumor growth inhibition of LLC after treatment with the angiostatic chemokine CXCL4L1. LLC cells were subcutaneously implanted in C57Bl/6 mice in 2 separate experiments with different settings (first experiment 40 wt and 20 CXCR3^−/− mice, ie, n = 10 per group; second experiment 90 wt and 30 CXCR3^−/− mice; ie, n = 15 per group). In the first experiment, 6 treatment groups were included (control [Ctrl] versus CXCL4L1 normal goat serum-treated; Ctrl versus CXCL4L1 anti-CXCR3-treated; and Ctrl versus CXCL4L1 in CXCR3^−/− mice). In the second experiment, 2 additional control groups of wt mice (WT Ctrl and WT CXCL4L1) were included that received no antibody treatment. Intratumoral chemokine treatment (vehicle control or 0.1 μg human CXCL4L1 per injection) started at the time of tumor inoculation and was repeated 3 times a week. Neutralization of CXCR3 was obtained by intraperitoneal injection of 0.5 mL polyclonal antiserum (4 mg immunoglobulin), 3× a week, starting at the time of tumor inoculation. Tumor dimensions were measured every week (A-C). (A-B) The mean tumor size (mm³) ± SEM per group from the second experiment. (C) The statistical analysis of the tumor sizes after 3 weeks when data from both experiments were combined. The WT Ctrl and WT CXCL4L1 group are not shown, because these treatments were only tested in the second experiment. To assess tumor vascularity, 5 tumors per group from both experiments were minced into single-cell suspensions for flow cytometric analysis using Abs against the endothelial cell marker MECA32 (panel D, n = 10/group). Statistically significant differences between the indicated groups were determined by the Mann Whitney test (*P < .05; **P < .01).