Medical Microbiology

witherythrocytesfromtheprospectiverecipient.Toensurenoreaction

followingtransfusion,thereshouldbenoagglutinationpresentineither

mixture.Somepotentiallydangerousserumantibodiesmaybindtotheer-

ythrocytescausingopsonization,butnotnecessarilyinducingagglutination.

Tocheckforthepresenceofsuchantibodies,anti-humanimmunoglobulin

serumisaddedandshoulditcrosslinksuchantibodiesagglutinationwill

result.

TypeIII:DiseasesCausedbyImmuneComplexes........

Pathologiesinitiatedbyimmunecomplexesresultfromthedepositionof

small,soluble,antigen-antibodycomplexeswithintissues.Themainhall-

markofsuchreactionsisinflammationwiththeinvolvementofcomple-

ment.Normally,largeantigen-antibodycomplexes(thatis,thoseproduced

inequivalence)arereadilyremovedbythephagocytesofthereticuloendo-

thelialsystem.Occasionally,however—especiallyinthepresenceofpersistent

bacterial,viral,orenvironmental,antigens(e.g.,fungalspores,vegetableor

animalmaterials),orduringautoimmunediseasesdirectedagainstautoanti-

gens(e.g.,DNA,hormones,collagen,IgG)whereautoantibodiestothebody’s

ownantigensareproducedcontinuously—depositionofantigen-antibody

complexesmaybecomewidespreadoftenbeingpresentonactivesecretory

membranesandwithinsmallervessels.Suchprocessesaremainlyobserved

withininfectedorgans,butcanalsooccurwithinkidneys,joints,arteries,skin

andlung,orwithinthebrain’splexuschoroideus.Theresultinginflammation

causeslocaltissuedamage.Mostimportantly,activationofcomplement

bysuchcomplexesresultsinproductionofinflammatoryCcomponents

(C3aandC5a).Someoftheseanaphylatoxinscausethereleaseofvasoactive

amineswhichincreasevascularpermeability(seealsop. 1 03f.).Additional

chemotacticactivitiesattractsgranulocyteswhichattempttophagocytize

thecomplexes.Whenthesephagocytesdie,theirlysosomalhydrolyticen-

zymesarereleasedandcausefurthertissuedamage.Thisprocesscanresult

inlong-termchronicinflammatoryreactions.

Therearetwobasicpatternsofimmunecomplexpathogenesis:

&Immunecomplexesinthepresenceofantigenexcess.Theacuteform
ofthisdiseaseresultsinserumsickness,thechronicformleadstothede-
velopmentofarthritisorglomerulonephritis.Serumsicknessoftenresulted
fromserumtherapyusedduringthepre-antibioticera,butnowonlyoccurs
rarely.Inoculationwithequineantibodiesdirectedagainsthumanpathogens,
orbacterialtoxins,ofteninducedtheproductionofhost(human)antibodies
againsttheequineserum.Becauserelativelylargeamountsofequineserum
wereadministeredforsuchtherapeuticpurposes,suchtherapywouldresult

ThePathologicalImmuneResponse 113

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Kayser, Medical Microbiology © 2005 Thieme

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