简介：EfficientactivationofTlymphocytesthroughTcellreceptor(TCR)dependsontwosignals．Thefirstsignal(signalone)isderivedfromTCRinteractingwiththeMHC／antigenicpeptidecomplex，whichconfersantigenicspecificitytotheimmuneresponse．Thesecondsignal(signaltwo)isprovidedbytheengagementofTcellsurfacereceptorswiththeirspecificligandsonantigenpresentingcell(APC)[1]．Asthereisgrowingevidenceforbidirectionalcommunicationsandsocalled“reversesignaling”fortraditionallydefinedligands，thedistinctionbetweenreceptorsandligandsbecomeslessclear．Thesepairsofmoleculesshouldbeviewedascosignalingmoleculesfunctioningincellswhichwouldexpresseitherthereceptorsortheligands.

简介：Toinvestigatewhetherestradiol(E2)playsaroleincell-contact-dependentregulatorymechanismofTcellactivation,westudiedtheroleofE2inregulatinggenetranscriptionofCTLA-4,ICOS,B7-1,B7-2andB7hinvitro.ThespleniccellsofnormalfemaleBALB/cmicewereactivatedbyConA.ThenthecellswereculturedwithE2(100pg/mlor50ng/ml)for24hor48h,respectively.ThecellproliferationwasmeasuredbyMTTassayandtheexpressionoftheco-stimulatorymoleculesmRNAwasexaminedbyRT-PCRanalysis.WefoundthatE2(100pg/ml,physiologicallevel)stimulatedtheactivatedspleencellsproliferation;inhibitedCTLA-4,ICOS,TGF-βandIL-10genetranscription;promotedB7-1andB7-2genetranscription.E2(50ng/ml,pregnantlevel)inhibitedtheproliferationoftheactivatedspleniccells;promotedCTLA-4,B7-1,IL-10butinhibitedB7-2andTGF-βgenetranscription.Therefore,weconcludethattheeffectsofE2onTcellactivationarepartiallythroughitsregulationontheco-stimulatorymolecules.Theco-stimulatorymoleculesarecrucialcomponentsofthecell-contactdependentregulatorymechanism,andE2mayregulateTcellactivationbythismechanism.