Figure 3. DC-HIL mediates T cell-suppressor activity of CD11b⁺Gr1⁺ cells.

(a, b) CGr1 cells from melanoma-bearing mice were cocultured with pmel-1 splenocytes (Spl), gp100 Ag, and anti-DC-HIL mAb (a), anti-coinhibitor Ab or control IgG (b). ³H-TdR incorporation measured. (c) Undepleted (DC-HIL⁺) or DC-HIL-depleted (DC-HIL^neg) CGr1 (Supplementary method) were assayed for suppression of pmel-1 splenocyte proliferation triggered by Ag (increasing ratios). (d) Mice (n=5) injected with pmel-1 CD8⁺ T-cells and DC-HIL⁺CGr1 or DC-HIL^negCGr1. Ten days after giving gp100, IFN-γ-producing cells in LN were counted. (e) Tumor growth following coinjection of DC-HIL⁺ or DC-HIL^neg CGr1 cells with B16 cells s.c. into naive mice (n=5). Using similar methods, DC-HIL^−/−CGr1 cells were compared with DCHIL^+/+ counterparts for DC-HIL expression by FACS (f), T-cell suppressing (g) and tumor-promoting ability (CD11b^neg cells as control) (h). *p<0.01.