Figure 2. Irf8-deficient mice harbor MDSC-like cells.

(A) Ability of CD11b⁺Gr-1⁺ cells isolated from WT or Irf8^–/– mice to inhibit anti-CD3–stimulated T cells at the indicated cell densities (n = 3 determinations, *P < 0.02; T cells plus anti-CD3 mAb control, average cpm, 127,151). (B) Ability of purified CD11b⁺Gr-1⁺ cells from Irf8^–/– mice to suppress alloreactive (H-2^b anti–H-2^d) T cell proliferation relative to the control, incubated with CD11b⁺Gr-1⁺ cells from WT mice. The CD11b⁺Gr-1⁺ cells matched the haplotype of the responder T cells and were tested at the indicated lymphocyte to myeloid cell ratios. Proliferation in A and B was measured through ³H-thymidine uptake and is representative of 2 separate experiments. (C) AT-3 tumor cells were co-mixed with or without CD11b⁺Gr-1⁺ cells derived from Irf8^–/– mice, and tumor growth was recorded. The results represent the mean ± SEM (n = 8 recipient mice/group pooled from 2 separate experiments; *P = 0.002). (D) AT-3 tumor growth rate in WT versus Irf8^–/– mice (n = 5 recipient mice/group; P = 0.02).