Medical Microbiology

andmastcellshaveahalf-lifeofseveralmonthsandwhenboundbythespe-
cificallergenmediatecellulardegranulationandthereleaseofbiogenic
amines(e.g.,histamine,serotonin).These mediators caninfluence the
smoothmusculature,andmainlyresultintheconstrictionofthepulmonary-
andbroncho-postcapillaryvenules,togetherwitharterioledilation.Thelocal
manifestationsofIgE-triggeredanaphylaxisincludewhealingoftheskin(ur-
ticaria),diarrheaforfoodallergies,rhinitisorasthmaforpollenallergies,ora
generalizedanaphylacticshock.IgEreactionsareusuallymeasuredinvitro
usingRIA(radioimmunoassay),RIST(radioimmunosorbenttest)orRAST
(radioallergosorbenttest)(seeFig.2. 28 andFig.2. 29 ,p. 13 1f.)Frequentcausal
agentsofIgEallergiesinhumansincludepollen,animalhair,housedust
(mites),insectbitesandstings,penicillin,andfoods.Examplesofallergicdis-
easesincludelocalallergicrhinitisandconjunctivitis,allergicbronchialasth-
ma,systemicanaphylacticshock,insecttoxinallergies,housedust(mite)and
foodallergies,urticaria,andangioedemas.
Degranulationofmastcellsandbasophilscanbeinducedbyfactors
otherthanthecross-linkingofspecificIgEantibodies.Suchfactorsinclude
thecomplement factors C3a and C5a, and pharmacological inducers
(“pseudo-allergy!”).
Atopicpatientssufferseverelyfromallergies.Atopiaisgeneticallycondi-
tioned,withachildexhibitinga 50 %riskofdevelopingatopyifbothparents
areallergic,ora 30 %riskifonlyoneparentisallergic.Theincidencelevelof
atopywithinthegeneralpopulationisroughly 10 – 15 %.Atopiacorrelates
withhighlevelsofIgEproduction,anddesensitizationreferstoattempts
tochangeaTH2(IgE-producing)responseintoaTH1(IgG-favoring)response
bymeansofrepeatedinoculationsororaldosesofallergens(seeFig.2. 14 ,
p.78).ItislikelythatincreasedproductionofIgG—asopposedtoIgE—anti-
bodiesplaysamajorroleinthesuccessofdesensitization.IgEnodoubthasan
importantbiologicalfunction,probablyagainstectoparasites,withallergic
reactionsrepresentingnothingmorethananunfortunatesideeffectof
thisbiologicalsystem.Littleresearchhasbeenperformedonthenatureof
theprotectivefunctionofIgEduringparasiticinfections(orontheroleof
eosinophils).However,wedoknowthatmediatorsreleasedbyIgE-triggering
ofmastcellsandbasophilscausethesmoothintestinalmusculaturetocon-
tract,andinthiswayfacilitatetheeliminationofintestinalparasites.

TypeII:CytotoxicHumoralImmuneResponses..........

ThesearepathologicalimmuneresponsesinducedbythebindingofIgM
orIgGantibodiestoantigenspresentonacellsurface(includingviralpro-
ductsorhaptens),orwithintissuecomponents.Themediatorsresponsible
forsuchtissuedamageareusuallycomponentsofthecomplementsystem,

ThePathologicalImmuneResponse 109

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