&IgE-mediateddefenseisimportant,alongwithIgA,inenhancingtheeli-
minationofgastrointestinal,pulmonary,anddermalparasites.Althoughde-
tailsoftheprocessarestillsketchy,IgE-dependentbasophilandeosinophil
defensemechanismshavebeendescribedformodelschistosomalinfections.
ImmuneDefensesagainstInfectionandTumorImmunity 101
GeneralSchemesofInfectiousDiseases
Fig.2. 19 Thedegreeofhostsurvivaldependsonboththerateofproliferation,
andtheextentofspread,ofaninfectiousagent–aswellastheintensityofthe
host’scytotoxicT-cellresponse.Infectionbycytopathicpathogenscanonlybe
controlledifpathogenicproliferationisslowandthepathogenremainslocalized;
otherwisetheoutcomeisusuallyfatal.Inthecaseofnoncytopathicpathogens,
thecytotoxicT-cellresponseisthecriticalparameter.Pathogenswhichproliferate
slowlyarequicklyeradicated.TheT-cellresponsecanbehaltedbypathogens
whichproliferaterapidlyandspreadwidelyduetothedeletionofresponding
Tcells.Thedegreeofsurvivalforhostsishighinbothofthesecases.Forpathogens
whichexhibitmoderateratesofproliferationandspread,theT-cellresponsemay
causeextensiveimmunopathologicaldamage,andthusreducetheproportionof
survivinghosts,someofwhichwillcontrollvirus,somenot.
Aweakenedimmunedefensesystemmaynotprogressbeyondanunfavorable
virus-hostbalance,evenwhenconfrontedwithastaticorslowlyreplicatingpatho-
genwhichrepresentsaninitiallyfavorablebalance.
2
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Kayser, Medical Microbiology © 2005 Thieme
All rights reserved. Usage subject to terms and conditions of license.