Figure 5.
The mAb 1C9 protects PNH RBCs in vitro and prevents complement-mediated intravascular hemolysis in vivo in a mouse model. (A) RBCs from a PNH patient were incubated with 50% acidified NHS in the presence of 0 to 1500 nM of 1C9 or 5 mM of EDTA (control [Ctrl]). After incubation, surviving PNH RBCs (CD59−) were quantitated by flow cytometry. Representative results from 2 repetitive experiments. (B) NHS was mixed with 1C9 or mouse IgG (mIgG) and then immediately injected IV into WT C57BL/6 mice via the tail vein. After 10 minutes, blood samples were collected in EDTA-containing tubes via terminal retroorbital bleeding. In vivo intravascular hemolysis was measured in the plasma by reading the optical density at 450 nm (OD450). Each dot presents 1 mouse. Ctrl were naïve C57BL/7 mice. *P < .05.

The mAb 1C9 protects PNH RBCs in vitro and prevents complement-mediated intravascular hemolysis in vivo in a mouse model. (A) RBCs from a PNH patient were incubated with 50% acidified NHS in the presence of 0 to 1500 nM of 1C9 or 5 mM of EDTA (control [Ctrl]). After incubation, surviving PNH RBCs (CD59) were quantitated by flow cytometry. Representative results from 2 repetitive experiments. (B) NHS was mixed with 1C9 or mouse IgG (mIgG) and then immediately injected IV into WT C57BL/6 mice via the tail vein. After 10 minutes, blood samples were collected in EDTA-containing tubes via terminal retroorbital bleeding. In vivo intravascular hemolysis was measured in the plasma by reading the optical density at 450 nm (OD450). Each dot presents 1 mouse. Ctrl were naïve C57BL/7 mice. *P < .05.

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