Figure 3 from GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling
Year: 2025
Type: other
Abstract: GPR65 KO tumors drive CAR T resistance in vivo without reducing cognate antigen expression or CAR T-cell expansion. A and B, Mice received 1 × 106 m.CR or GPR65 KO tumor cells on day 0, followed by treatment with 10 × 106 CAR T cells or PBS 7 days later. A, Bioluminescence imaging showing tumor growth. Representative of three experiments, with n = 5 mice per group. B, Kaplan–Meier survival curves. Statistical significance was calculated using the log-rank (Mantel–Cox) test. Pooled from three experiments, n = 15 mice per group. C and D, Mice received 1 × 106 GPR65 KO1 or GPR65 KO1 OE tumor cells, followed by treatment with 10 × 106 CAR T cells or PBS 7 days later. C, Bioluminescence imaging showing tumor growth. Representative of two experiments, with n = 5 mice per group. OE, overexpression. D, Kaplan–Meier survival curves. Significance was determined using the log-rank (Mantel–Cox) test. Pooled from two experiments, with n = 10 mice per group. E and F, Spleen, bone marrow, and liver were harvested 4 days after CAR T treatment, and tumor and CAR T cells were analyzed by flow cytometry. E, Tumor cell percentage and number. F, CAR T-cell percentage and number. Representative of three experiments, with n = 3–5 mice per group. Significance was determined by one-way ANOVA with the Tukey post hoc test for multiple comparisons. Error bars represent mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
Language: English
Topic: CAR-T cell therapy research
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
OpenAlex ID: W4410047606