By Henry G. Kunkel and Frank J. Dixon (Eds.)
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Only limited information is available at present on the extent to which nucleated mammalian cells including tumor cells are susceptible to this mechanism of eradication. , 1974). , 1976; Theofilopoulos and Perrin, 1976). Activation of the pathway resulted in Raji cell lysis, although up to 24 hours of incubation was required for lysis to reach completion (Theofilopoulos and Perrin, 1977). , 1977). Activation and lysis were shown to be independent of antibody by use of either preabsorbed serum or hypogammaglobulinemic serum.
The large lag between occurrence of the initial membrane lesion and cell lysis may be due to cellular defense against complement attack. This assumption is supported by disappearance of the lag following inhibition of cell metabolism. Nevertheless, it is remarkable that 90,000 C9 molecules per cell corresponding to 15,000 MAC are not capable of effecting rapid cell death. Temporal resistance to lysis may be due not only to cellular defense, but also to the rate of MAC accumulation on ALTERNATIVE PATHWAY OF COMPLEMENT 37 the target cell.
When bound to an activator, the ability of C3b to bind P1H is diminished and, consequently, formation of C 3 convertase (C3b,Bb) and amplification commence. , 1976a,c). , 1978). The active site responsible for C 3 and C 5 cleavage resides in the Bb subunit of the enzyme. , ALTERNATIVE PATHWAY OF COMPLEMENT 29 1976a). , 1976a,c). , 1977)Binding-activation of properdin results in stabilization of the enzyme such that its half-life at 37°C increases to 10 minutes. ” This form is able to bind to C3b directly without the aid of factor B, but it retains the ability to stabilize the preformed enzyme.
Advances in Immunology, Vol. 29 by Henry G. Kunkel and Frank J. Dixon (Eds.)