THE CONTROL OF HOMOLOGOUS LYSIS
THE CONTROL OF HOMOLOGOUS LYSIS
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DOI:
10.1016/0167-5699(91)90005-e
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发表时间:
1991-09-01
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影响因子:
--
通讯作者:
LACHMANN, PJ
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文献类型:
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作者:
LACHMANN, PJ
Complement activation unleashes powerful effector mechanisms against which host cells are protected by homologous restriction factors. These factors are glycolipid-anchored membrane proteins that either induce C3 convertase dissociation (for example decay-accelerating factor) or prevent the full development of the membrane attack complex (for example homologous restriction factor and CD59). In this article Peter Lachmann explores the biology and biochemistry of these important and intriguing molecules.In the complement lysis of antibody-coated red blood cells, a degree of specificity exists for the species of red blood cell lysed by a particular species of complement. A dramatic example of this is the failure of horse or ox complement to lyse antibody-coated sheep or ox red blood cells, whereas complement from both sources is lytic to guinea-pig red blood cells. Thus, although this specificity is not a genuine self-nonself discrimination, complement of a given species is relatively inefficient at lysing its own cells. This phenomenon was already known by the earliest complement workers who used nonlytic'agglutinating'complement to measure conglutination reactions 1. The term'homologous restriction'is now used for this phenomenon. In recent years, it has become apparent that a number of phenomena contribute to homologous restriction, acting in different ways and at various stages of complement activity.