Activators of the alternative pathway of complement such as zymosan, rabbit erythrocytes, and heat-killed E. coli protect bound C3b from C3bINA and P, C3b, Bb from decay-dissociation by β1H, thereby amplifying C3b generation and deposition. The capacity of purified components and control proteins to modulate alternative pathway activation by zymosan and rabbit erythrocytes (Er) was assessed in dilute C2-deficient human serum.

Zymosan-induced inactivation of C3 and B was determined at different intervals after 100 µg of zymosan were added to 150 µl of serum diluted 1:6 in VBS++. The mean inactivation of C3 and B at 45 minutes was 61 ± 5.4% (±1 SD) and 62 ± 5.7%, respectively. Various amounts of the control proteins were added to the serum to determine the increase over endogenous concentrations necessary to inhibit 50% of the zymosan effect. Increases of C3bINA by 43% and of β1H by 25% inhibited 50% of zymosan-induced inactivation of C3.

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