Figure 5.
Anti-Ly6G Ab–mediated G-MDSC depletion accelerates BM damage in the MHC-mismatched CByB6F1 AA model. (A) LN cells extracted from B6 donor mice were injected into 5 Gy TBI pretreated CByB6F1 recipients. Some recipients also received intraperitoneal injection of anti-mouse Ly6G antibody at 500 μg/mouse to deplete G-MDSCs. (B) At 2 weeks, clearance of Ly6G+ cells in BM of antibody-injected animals was confirmed by flow cytometry. (C) At this time point, there was worse neutropenia, anemia, and thrombocytopenia in peripheral blood and BM hypoplasia in anti-Ly6G antibody–injected BMF mice (n = 18) than in control BMF mice without antibody injection (n = 18), as well as increased CD4 and CD8 T-cell infiltration in the BM. Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

Anti-Ly6G Ab–mediated G-MDSC depletion accelerates BM damage in the MHC-mismatched CByB6F1 AA model. (A) LN cells extracted from B6 donor mice were injected into 5 Gy TBI pretreated CByB6F1 recipients. Some recipients also received intraperitoneal injection of anti-mouse Ly6G antibody at 500 μg/mouse to deplete G-MDSCs. (B) At 2 weeks, clearance of Ly6G+ cells in BM of antibody-injected animals was confirmed by flow cytometry. (C) At this time point, there was worse neutropenia, anemia, and thrombocytopenia in peripheral blood and BM hypoplasia in anti-Ly6G antibody–injected BMF mice (n = 18) than in control BMF mice without antibody injection (n = 18), as well as increased CD4 and CD8 T-cell infiltration in the BM. Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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