The control of homologous lysis.
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.
Lachmann
P J
PJ
Molecular Immunopathology Unit, MRC Centre, Cambridge, UK.
D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D018957:CD59 Antigens; D050577:Complement C3-C5 Convertases / Q000276:immunology; D003185:Complement C8 / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology*; D006457:Hemoglobinuria, Paroxysmal / Q000276:immunology; D006461:Hemolysis / Q000276:immunology*; D006801:Humans; D008562:Membrane Glycoproteins / Q000276:immunology; D011951:Receptors, Complement / Q000276:immunology
D015703:Antigens, CD; D018957:CD59 Antigens; D003185:Complement C8; D008562:Membrane Glycoproteins; D011951:Receptors, Complement; D003165:Complement System Proteins; D050577:Complement C3-C5 Convertases