Fig. 3.
Fig. 3. Binding of autologous IgG (A) and complement C3 fragments (B) in normal and deficient NPE, RPE, and TPE. Normal and deficient parasitized E were fractionated from asynchronous cultures by the Percoll-mannitol method. After opsonization with fresh autologous serum and washings, parasitized E and nonparasitized controls were incubated with [125I] Protein A, or with [125I] anti-C3c antibodies and their binding assayed as indicated. Binding of molecules is expressed as number of [125I] Protein A molecules per cell (as measure of autologous IgG binding) or as cpm of [125I] anti-C3c antibodies bound per 1,000 cells (as measure of complement C3 fragments binding). Mean values ± SD of five separate experiments. Data obtained with separated RPE fractions that contained 30% to 45% RPE were extrapolated to 100% RPE parasitemia as detailed in Materials and Methods. Data obtained with separated TPE fractions (>95% TPE) were not extrapolated to 100% TPE parasitemia. Binding of autologous IgG binding: difference of normal RPE versus deficient RPE: P = .001; normal TPE versus deficient TPE:P = .39. Binding of complement C3 fragments: difference of normal RPE versus deficient RPE: P = .006; normal TPE versus deficient TPE: P = .004. Significance of differences was assessed by t-test for paired samples.

Binding of autologous IgG (A) and complement C3 fragments (B) in normal and deficient NPE, RPE, and TPE. Normal and deficient parasitized E were fractionated from asynchronous cultures by the Percoll-mannitol method. After opsonization with fresh autologous serum and washings, parasitized E and nonparasitized controls were incubated with [125I] Protein A, or with [125I] anti-C3c antibodies and their binding assayed as indicated. Binding of molecules is expressed as number of [125I] Protein A molecules per cell (as measure of autologous IgG binding) or as cpm of [125I] anti-C3c antibodies bound per 1,000 cells (as measure of complement C3 fragments binding). Mean values ± SD of five separate experiments. Data obtained with separated RPE fractions that contained 30% to 45% RPE were extrapolated to 100% RPE parasitemia as detailed in Materials and Methods. Data obtained with separated TPE fractions (>95% TPE) were not extrapolated to 100% TPE parasitemia. Binding of autologous IgG binding: difference of normal RPE versus deficient RPE: P = .001; normal TPE versus deficient TPE:P = .39. Binding of complement C3 fragments: difference of normal RPE versus deficient RPE: P = .006; normal TPE versus deficient TPE: P = .004. Significance of differences was assessed by t-test for paired samples.

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