Figure 6.
Anti-Ly6G Ab mediates intermediate Ly6G+cell expansion, resulting in mild attenuation of marrow failure in minor histocompatibility–mismatched C.B10 AA model. (A) Anti-Ly6G antibody was injected into a minor histocompatibility (minor-H)–mismatched C.B10 BMF model at the time of LN infusion. Anti-Ly6G antibody improved PLTs (B), reduced BM CD8 T-cell frequency (C) with no change in total BM cell recovery. (D) Anti-Ly6G antibody treatment promoted generation of a new Ly6ClowCD11b+ cell population with intermediate Ly6G expression. (E) Ly6G intermediate population showed similar immunosuppressive function as did G-MDSCs from normal control mice. The function assay was duplicated. BMF control group (n = 12), BMF+anti-Ly6G antibody group (n = 12). Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001.

Anti-Ly6G Ab mediates intermediate Ly6G+cell expansion, resulting in mild attenuation of marrow failure in minor histocompatibility–mismatched C.B10 AA model. (A) Anti-Ly6G antibody was injected into a minor histocompatibility (minor-H)–mismatched C.B10 BMF model at the time of LN infusion. Anti-Ly6G antibody improved PLTs (B), reduced BM CD8 T-cell frequency (C) with no change in total BM cell recovery. (D) Anti-Ly6G antibody treatment promoted generation of a new Ly6ClowCD11b+ cell population with intermediate Ly6G expression. (E) Ly6G intermediate population showed similar immunosuppressive function as did G-MDSCs from normal control mice. The function assay was duplicated. BMF control group (n = 12), BMF+anti-Ly6G antibody group (n = 12). Data are shown as means with standard errors. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001.

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