Human serum deficient in C2 was studied for opsonic activity by using test strains of Escherichia coli, Proteus mirabilis, Staphylococcus aureus and Diplococcus pneumoniae in an in vitro system of phagocytosis and bacterial killing. Heat labile opsonic activity was apparently effected through the alternate C3–C9 pathway since absorption of fresh serum with inulin at 37°C abolished opsonic activity concurrent with β1c to β1a conversion. The same treatment was shown to activate the C3 activator system. In addition, activation of C3 with isolated 140,000 m.w. cobra venom factor resulted in loss of opsonic activity for test organisms. The alternate complement activation pathway may be important in the opsonic functions necessary for in vivo phagocytosis of organisms.

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