Figure 2.
Complement, in contrast to FcγRs, is essential for in vivo antibody-mediated TRALI induction. C5-deficient (A-B) and BALB/c WT mice (C-D) were primed as described in Figure 1. (A,C) Rectal temperatures and (B,D) lung W/D weight ratios after 90 minutes of antibody infusion (C5-deficient mice: 4.5 mg/kg IV; BALB/c WT mice: 1 mg/kg IV). All human antibodies (C-D) were hIgG1 chimeric variants. Variants used were K322A (no C1q binding), ΔG236 (no FcγR binding), and PGLALA (no C1q/FcγR binding). Only statistical differences of interest are shown; each dot represents 1 mouse. n = 6; rectal temperatures: n = 2 for 34-1-2S–hIgG1; n = 5 for 34-1-2S and for 34-1-2S–ΔG236 because of reaching humane end points; other groups, n = 6. Data are shown as means ± SD; ∗∗∗∗P < .0001. Statistical analysis was performed with a one-way ANOVA with a Tukey post hoc test. NS, nonsignificant.

Complement, in contrast to FcγRs, is essential for in vivo antibody-mediated TRALI induction. C5-deficient (A-B) and BALB/c WT mice (C-D) were primed as described in Figure 1. (A,C) Rectal temperatures and (B,D) lung W/D weight ratios after 90 minutes of antibody infusion (C5-deficient mice: 4.5 mg/kg IV; BALB/c WT mice: 1 mg/kg IV). All human antibodies (C-D) were hIgG1 chimeric variants. Variants used were K322A (no C1q binding), ΔG236 (no FcγR binding), and PGLALA (no C1q/FcγR binding). Only statistical differences of interest are shown; each dot represents 1 mouse. n = 6; rectal temperatures: n = 2 for 34-1-2S–hIgG1; n = 5 for 34-1-2S and for 34-1-2S–ΔG236 because of reaching humane end points; other groups, n = 6. Data are shown as means ± SD; ∗∗∗∗P < .0001. Statistical analysis was performed with a one-way ANOVA with a Tukey post hoc test. NS, nonsignificant.

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