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1、258infusion,indicatingthatthesenodeshaveasignificantroleinsystemicimmunization.(SupportedbyUSPHSGrantNS-11050.)RoleofCellularImmuneFactorsinCoronavirusA59InducedDemyelination.M.J.M.Koolen*,M.J.BuchmeierandC.J.Lucas*.(Dept.ofImmunology,ScrippsClinicandResearchF
2、oundation,LaJolla,CA,and*CentralLabNetherlandsRedCrossBloodTransfusionService,incorporatingtheLabofExpandClinImmunologyoftheUniversityofAmsterdam,Amsterdam,TheNetherlands)Cellularimmunefactorsinvolvedinmousehepatitisvirus(MHV)strainA59andatemperature-sensitive
3、mutant(ts-342)-induceddemyelinationwerestudiedinnormalandathymicnu/nuBALB/cmiceaswellasinmicedepletedofaspecificsubsetofTlymphocytesinvivo.IntracerebralinoculationofnormalBALB/cmicewith10"5PFUofts-342resultedinprolongedinfectionofthecentralnervoussystem,wherea
4、s100PFUofthewildtypeviruswerelethal.Inathymicnu/numice,bothwildtypevirusandts-342causedafatalhepatitissuggestingthatcellularimmunefactorsareinvolvedintheprotectionofmiceagainstlethalMHV-infection.Furthermore,significantlevelsofproliferation,measuredas3H-thymid
5、ineincorporation,wereobservedwhensplenocytesisolatedfromts-342infectednormalmicewereculturedinthepresenceofeitherviralantigenormyelinbasicprotein(MBP).TherespondercellswereshowntobeTlymphocytes,andinvivodepletionoftheL3T4populationreducedtheprolifeativerespons
6、etoMBPtobaselinelevels.lmmunoblotAnalysisofAntiAChRAntibodiesinMyastheniaGravis.R.Mantegazza,P.Romagnoli,F.Baggi,O.Simoncini,D.Neumann*,F.CornelioandS.Fuchs*.(Dept.ofneuromuscularDisease,Milan,Italyand*Dept.ofChemicalImmunology,TheWeizmannInstituteofScience,Re
7、hovot,Israel)Finespecificityofantiacetylcholinereceptorantibodies(a-AChR-Abs)inMyastheniaGravis(MG)andtheirrelationshiptothepathogenesisarenotcompletelydefined,BythemeanofimmunoblottingtechniqueswetriedtoachievemoreinsightinthecompositionofthedifferentAb-subpo
8、pulations.AChRfromTorpedoCalifornia(T-AChR)waspurified,blottedontonitrocellulosepaper,probedwithserafrompatientsindifferentclinicalconditionsandrevealedonautoradiographybymeansofPr
