Fig. 8: Blockage of VCAM1-CD49d signaling enhances anti-tumor efficacy of iNKT cells.

a Timeline of experimental procedure for (b–d). b–d Picture (b), weight (c), and growth curves (d) of Vcam1 knockdown MC38 tumors and NTC MC38 tumors in WT mice receiving iNKT cells plus αGC or receiving PBS buffer (n = 9–10 mice per group). e Timeline of experimental procedure for (f–j). f–g Picture (f) and weight (g, n = 8 mice per group) of MC38 tumors in WT mice receiving iNKT cells plus αGC combined with anti-CD49d antibody or IgG isotype control antibody. h Growth curves of MC38 tumors in WT mice receiving anti-CD49d antibody or IgG isotype control antibody in combination with (n = 8 mice per group) or without (n = 6 mice per group) iNKT cells plus αGC. i, j Frequencies (i) and IFN-γ production (j) of total iNKT cells, CD8 T cells, and NK cells in MC38 tumors described in (f, g). k VCAM1 expression in DCs, macrophages (Mø), monocytes, and tumor cells in B16F10 tumors from WT mice (n = 5 mice). l Timeline of experimental procedure for (m–q). m–q Picture (m), weight (n), and growth curves (o) of B16F10 tumors in WT mice receiving iNKT cells plus αGC combined with anti-VCAM1 antibody or anti-CD49d antibody or IgG isotype control antibody (n = 5 mice per group). p, q Frequencies (p) and IFN-γ production (q) of total iNKT cells, CD8 T cells, and NK cells in B16F10 tumors described in (m-o). r Timeline of experimental procedure for (s–u). NTC, none target control. s–u Picture (s), weight (t), and growth curves (u) of Vcam1 knockdown MC38 tumors and NTC MC38 tumors with or without CD1d overexpression in WT mice receiving iNKT cells plus αGC (n = 7 mice per group). Data are represented as mean ± SEM, and were analyzed by one-way ANOVA (c, k, n, p, q, t), two-way ANOVA (d, h, o, u), and two-tailed unpaired Student’s t-test (g, i, j). Source data are provided as a Source Data file.