Figure 2.
As therapy, G-MDSCs attenuate BMF in minor histocompatibility–mismatched C.B10 mice. (A) G-MDSCs were injected at day 3 after LN cell infusion in the C.B10 BMF model. (B) Relative to BMF controls, G-MDSC–treated mice (n = 12) had higher WBCs, RBCs, HGB, PLTs, and total BM cells at day 14 following model initiation relative to untreated BMF mice (n = 9). (C) G-MDSCs decreased CD4 and CD8 T-cell infiltration of BM. (D) G-MDSCs decreased Fas expression and Annexin V binding of residual BM cells (RBMs). (E) G-MDSCs suppressed intracellular levels of IFN-γ and TNF-α, as well as cell proliferation protein Ki67 in BM CD4 and CD8 T cells relative to BMF control mice. (F) The correlations of BM G-MDSCs with WBC, RBC, and PLT in peripheral blood and RBM, CD4% T cells, and CD8% T cells in the BM were analyzed by linear regression. Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

As therapy, G-MDSCs attenuate BMF in minor histocompatibility–mismatched C.B10 mice. (A) G-MDSCs were injected at day 3 after LN cell infusion in the C.B10 BMF model. (B) Relative to BMF controls, G-MDSC–treated mice (n = 12) had higher WBCs, RBCs, HGB, PLTs, and total BM cells at day 14 following model initiation relative to untreated BMF mice (n = 9). (C) G-MDSCs decreased CD4 and CD8 T-cell infiltration of BM. (D) G-MDSCs decreased Fas expression and Annexin V binding of residual BM cells (RBMs). (E) G-MDSCs suppressed intracellular levels of IFN-γ and TNF-α, as well as cell proliferation protein Ki67 in BM CD4 and CD8 T cells relative to BMF control mice. (F) The correlations of BM G-MDSCs with WBC, RBC, and PLT in peripheral blood and RBM, CD4% T cells, and CD8% T cells in the BM were analyzed by linear regression. Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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