Figure 1
Figure 1. Improved human hematopoietic cell engraftment in NOD/SCID mice by intravenous administration of NAC. NOD/SCID mice were injected with NAC or phosphate-buffered saline (control group) for 2 consecutive weeks. The NAC-injected mice also received NAC in their drinking water until the termination of the experiments. NAC-treated and untreated recipients were transplanted with human CD34+ CB cells intravenously, and human chimerism was assessed by flow cytometry in the BM and spleen. (A) Representative profile of 2′,7′-dichlorofluorescin diacetate–stained BM cells isolated from age-matched C57BL/6, BALB/C, NAC-treated, and untreated NOD/SCID mice. (B) Mean for replicates of (A) shown in BM cells (n = 10 mice per group; this analysis was consistent in 3 independent experiments). (C) Representative flow plots of human cell engraftment and multilineage differentiation in the BM and spleen of NAC-treated and untreated NOD/SCID mice engrafted with 5 × 105 CD34+ CB cells. (D,G) Mean engraftment levels of human cells in the BM and spleen of NAC-treated and untreated mice when different numbers (1 × 105, 2 × 105, 5 × 105, 6 × 105) of CD34+ CB cells were injected (for 1 × 105 and 2 × 105 cells: n = 15 mice per group, 3 independent experiments; for 5 × 105 cells: n = 14 mice per group, 3 experiments; for 6 × 105 cells: n = 8 mice per group, 2 experiments). (E,H) Bars represent the fold difference in engraftment levels between NAC-treated and untreated recipients in BM and spleen. (F) The CD34+CD38– population of the engrafting human cells (hCD45+) in NAC-treated and untreated recipient mouse BM. (I) Lineage engraftment of human cells. CD19+CD33– B cells, CD19–CD33+ myeloid cells, CD45–CD235a+ erythroid cells, CD56+ natural killer cells, and CD3+ T cells are shown. Values represent the mean ± standard error of the mean (SEM). *P < .05; **P = .01 to .001; ***P < .001. IgM, immunoglobulin M; SP, spleen.

Improved human hematopoietic cell engraftment in NOD/SCID mice by intravenous administration of NAC. NOD/SCID mice were injected with NAC or phosphate-buffered saline (control group) for 2 consecutive weeks. The NAC-injected mice also received NAC in their drinking water until the termination of the experiments. NAC-treated and untreated recipients were transplanted with human CD34+ CB cells intravenously, and human chimerism was assessed by flow cytometry in the BM and spleen. (A) Representative profile of 2′,7′-dichlorofluorescin diacetate–stained BM cells isolated from age-matched C57BL/6, BALB/C, NAC-treated, and untreated NOD/SCID mice. (B) Mean for replicates of (A) shown in BM cells (n = 10 mice per group; this analysis was consistent in 3 independent experiments). (C) Representative flow plots of human cell engraftment and multilineage differentiation in the BM and spleen of NAC-treated and untreated NOD/SCID mice engrafted with 5 × 105 CD34+ CB cells. (D,G) Mean engraftment levels of human cells in the BM and spleen of NAC-treated and untreated mice when different numbers (1 × 105, 2 × 105, 5 × 105, 6 × 105) of CD34+ CB cells were injected (for 1 × 105 and 2 × 105 cells: n = 15 mice per group, 3 independent experiments; for 5 × 105 cells: n = 14 mice per group, 3 experiments; for 6 × 105 cells: n = 8 mice per group, 2 experiments). (E,H) Bars represent the fold difference in engraftment levels between NAC-treated and untreated recipients in BM and spleen. (F) The CD34+CD38 population of the engrafting human cells (hCD45+) in NAC-treated and untreated recipient mouse BM. (I) Lineage engraftment of human cells. CD19+CD33 B cells, CD19CD33+ myeloid cells, CD45CD235a+ erythroid cells, CD56+ natural killer cells, and CD3+ T cells are shown. Values represent the mean ± standard error of the mean (SEM). *P < .05; **P = .01 to .001; ***P < .001. IgM, immunoglobulin M; SP, spleen.

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