By Henry G. Kunkel and Frank J. Dixon (Eds.)
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Additional info for Advances in Immunology, Vol. 29
The cellular mode of complement-dependent parasite killing operates through C3b. Owing to activation of the alternative pathway at the schistosomular surface, C3b becomes bound to the parasite. , 1978) and mast cells (Sher, 1976; Sher and McIntyre, 1977), which possess C3b receptors, have been shown in vitro to adhere to the C3b-coated organism. , 1978). Killing has not been demonstrated as yet for mast cells. , 1980). Phagocytosis is not accompanied by secretion of intracellular mediators or release of lysosomal enzymes.
1980). Two approaches were used. , 1979a). By and large, sialic acid in gly- 24 HANS J. MULLER-EBERHARD AND ROBERT D. SCHFWIBER coproteins is linked to galactose residues (Tooze, 1973). Removal of sialic acid would therefore reveal galactose and other neutral and amino sugars. , 1980). Incorporation of approximately 25,000 monomeric and base-hydrolyzed LPS structures (MW 10,000) per cell were needed to generate alternative pathway activating activity to the extent where 50% cytolysis occurred upon exposure to C4-depleted human serum.
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. If this rate is high, then Raji cells lyse within 1 hour (Podack and Muller-Eberhard, 1980). While evidence is accumulating showing that the alternative pathway operates without antibody, there are clear examples for antibody requirement in pathway-mediated cell lysis.
Advances in Immunology, Vol. 29 by Henry G. Kunkel and Frank J. Dixon (Eds.)