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JJ Houle, EM Hoffmann and AF Esser
Department of Comparative & Experimental Pathology, University of
Florida, Gainesville 32610.
Our previous work revealed that homologous complement (C) was ineffective
in lysing antibody-sensitized erythrocytes (EA) even at high
concentrations. It was also shown that activation of complement on
homologous EA resulted in the binding of C9 and the formation of EA bearing
complement proteins C1 through C9 (EAC1-9), yet few hemolytic sites were
formed. Instead, as shown here, the formation of homologous EAC1-9 caused
the cells to become resistant to lysis even by heterologous complement
during a second incubation. In contrast, when homologous EAC1-8 were
produced by incubating EA with C9-depleted serum, such intermediates were
not protected against lysis by heterologous complement during a second
incubation. Furthermore, homologous C9 on EAC1-9 was able to reduce the
hemolytic efficiency of heterologous complement without blocking C
activation and the formation of new C5b-9 complexes. Protection was not
modified when homologous EAC1-9 were produced in one step, by incubation of
EA with serum, or sequentially by adding C9 to EAC1-8. The minimum number
of 9-sites required to confer a protective effect on EAC1-9 was less than
200 per cell. Thus, in addition to its known effect in heterologous cell
killing, homologous C9 is capable of protecting homologous cells against
inadvertent complement lysis.
This article has been cited by other articles:
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| Copyright © 1988 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
