Figure 6.
NAC restores proliferation and metabolic reserve in cyclophosphamide-treated T cells. T cells from normal donors (n = 3) were exposed to cyclophosphamide, rescued with NAC, and then manufactured into CAR T cells targeting CD19 as previously described. We assessed CD107a degranulation against CD19 targets (Nalm-6) (A) as well as IFNγ production (B) in a 24-hour assay. There were no significant differences in short-term killing potential or cytokine release in the T cells that survived manufacture. Significant decreases with cyclophosphamide were seen in proliferation (C) during manufacture, however, with far fewer cell recovered. Peak blasting response measured by cell size (D) was also not affected. (E-F) NAC restores ECAR and OCR to near normal levels. Treatment with NAC restored proliferation and metabolic reserve. *P < .01. PMA+Ion, phorbol 12-myristate 13-acetate plus ionomycin.

NAC restores proliferation and metabolic reserve in cyclophosphamide-treated T cells. T cells from normal donors (n = 3) were exposed to cyclophosphamide, rescued with NAC, and then manufactured into CAR T cells targeting CD19 as previously described. We assessed CD107a degranulation against CD19 targets (Nalm-6) (A) as well as IFNγ production (B) in a 24-hour assay. There were no significant differences in short-term killing potential or cytokine release in the T cells that survived manufacture. Significant decreases with cyclophosphamide were seen in proliferation (C) during manufacture, however, with far fewer cell recovered. Peak blasting response measured by cell size (D) was also not affected. (E-F) NAC restores ECAR and OCR to near normal levels. Treatment with NAC restored proliferation and metabolic reserve. *P < .01. PMA+Ion, phorbol 12-myristate 13-acetate plus ionomycin.

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