Analysis of the Expression of Fas, FasL and Bcl-2 in the Pathogenesis of Autoimmune Thyroid Disorders

(整期优先)网络出版时间:2004-03-13
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Toinvestigatetheexpressionofapoptosis-relatedprotein(Fas,FasL,andBcl-2)inthepathogenesisofautoimmunethyroiddisorders(ATDs),immunohistochemicalstainingwasperformedon20Hashimoto'sthyroiditis(HT),20Graves'disease(GD),and20thyroidfollicularadenoma(TFA,ascontrol).AllthecasesexpressedFas,mainlyonthecellsurfaceandcytoplasm.FasLwasfoundin17casesoftheTFA.Bcl-2wasdetectedin15casesofHT,19ofGDand17ofTFA.InTFA,amoderateFasexpressionandaminimalornoFasLexpressionwasdetectedonfollicularcells.InHT,thefolliclesadjacenttoinfiltratinglymphocytesshowedincreasedlevelsofFasandFasLexpression.AweakerstainingofFasandFasLwasexhibitedoninfiltratinglymphocytesthanonthyrocytes.InacomparisonofGDwithHT,thyrocytesandlymphocytesshowedsimilarFasstaining,butforFasLthestainingwasratherweakerinHT.TheexpressionofBcl-2wasnearlyidenticalinGDandTFA,butmuchweakeronthefollicularcellsinvicinityoflymphocytesandonthelymphocyteslocatedingerminalcentersofHTtissues.TheexpressionofFas,FasL,Bcl-2inHashimoto'sthyroiditisandGraves'diseasewerealmostsame.FasLstrongexpressionandBcl-2weakexpressiononthefolliclesinHTmayinduceapoptosis.TheseresultsprovidedevidenceforexpressionofFas,FasLandBcl-2inthepathogenesisofautoimmunethyroiddisease.ThelymphocytesseemnottobedirectlyengagedintheprocessviatheirownFasL,buttheymayprovidesomecytokinesthat,inturn,upregulateFasand/orFasLexpressiontoinduceapoptosis.