Figure 2.
Anti-CD47/c-Kit plus ruxolitinib enables fully mismatched allo-HSCT, which corrects the defective phagocyte oxidative burst in the gp91phox–/Y mouse model of chronic granulomatous disease. Peripheral blood donor chimerism (top panels) and Dihydrorhodamine 123 staining after stimulation with phorbol 12-myristate-13-acetate (PMA) or treatment with dimethyl sulfoxide vehicle control (Unstim; bottom panels) in gp91phox–/Y mice transplanted as per the protocol in Figure 1A, using the indicated conditioning treatments (t = 3 months after HSCT, n = 4 mice per group). All plots are gated for CD11b+Gr1hi cells.

Anti-CD47/c-Kit plus ruxolitinib enables fully mismatched allo-HSCT, which corrects the defective phagocyte oxidative burst in the gp91phox–/Y mouse model of chronic granulomatous disease. Peripheral blood donor chimerism (top panels) and Dihydrorhodamine 123 staining after stimulation with phorbol 12-myristate-13-acetate (PMA) or treatment with dimethyl sulfoxide vehicle control (Unstim; bottom panels) in gp91phox/Y mice transplanted as per the protocol in Figure 1A, using the indicated conditioning treatments (t = 3 months after HSCT, n = 4 mice per group). All plots are gated for CD11b+Gr1hi cells.

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