Medical Microbiology

antibody-inducedcomplementactivationand“alternative”activationviaC3

(Fig.2. 16 ).

Duringclassicactivationofcomplement,C1qmustbeboundbyatleast

twoantigen-antibodyimmunecomplexes,towhichC4andC2thenattach

themselves.Together,thesethreecomponentsformaC3convertase,which

thensplitsC3.PentamericIgMrepresentsaparticularlyefficientCactivator

sinceatleasttwoIgFccomponentsincloseproximityarerequiredforC1q

bindingandactivation.

Duringalternativeactivationofcomplement,thesplittingofC3occurs

directlyviatheactionofproductsderivedfrommicroorganisms,endotoxins,

polysaccharides,oraggregatedIgA.C3b,whichisproducedinbothcases,is

activatedbythefactorsBandD,thenitselfactsasC3convertase.Subsequent

formationofthelyticcomplex,C5–C9(C5–9),isidenticalforbothclassic

88 2 BasicPrinciplesofImmunology

ImmunologicalCellDeath

Fig.2. 17 Oxygenradicalsandnitrousoxides(a),MACresultingfromcomplement

activation(b)andperforin(c)allcausemembranedamagewhichresultsincell

death.LigandbindingofFas/APO(d),interruptedsignalreceptorconduction(e),

corticosteroidbindingtoreceptorsandintracellularstructures(f),andDNAda-

mage(g)allresultinalterationsofintracellularsignalingcascadesandleadtocel-

lularapoptosis.(Fas=Fantigen;APO=apoptosisantigen;TNF=tumornecrosis

factor;Bcl2=B-cellleukemia-2antigen[aproteinthatinhibitsapoptosis].)

2

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Kayser, Medical Microbiology © 2005 Thieme

All rights reserved. Usage subject to terms and conditions of license.