简介：Ourpreviousstudiesshowedapredominanceofhighmolecularweightproteingroupintumornuclearmatrices.Contrarytonormalcells,proteinsofthisgrouparepreferentiallyphosphorylated.Phosphoproteinsofhepatomanuclearmatrixareselectivelysubjectedtorapidproteolysis.Byalkalitreatmentandamonoclonalantibodyagainstphosphotyrosylresiduethepresenceoftwohighmolecularweightbandsofphosphotyrosyl-containingproteinswasdetectedinnuclearmatricesoftumorbutnotofnormallivercells.Highmolecularweightproteingroupoftumornuclearmatricesrevealedalsoarapidturnoverandpreferentialincorporationoflabeledaminoacidsselectivelyinhibitedbychloramphenicol.

简介：Thl-responseplaysacrucialroleindeterminingpathogenesisoforgan-specificautoimmunediseases.ItisbelievedthatbothIL-12andINF-αareinitiatorstoregulateTh1-response.Inourexperimentalautoimmuneuveitis(EAU)model,bothLewisandFischer344ratssharethesameMHCclassⅡImolecules,whileLewisratisEAUsusceptibleandFischer344ratisEAUresistant.However,underthesameconditionofimmunization,ifpertussistoxin(PTX)wasinjectedintraperitoneallyasanadditionaladjuvant,Fischer344ratcandevelopEAU.InthisstudyweinvestigatewhichmechanismsareinvolvedintheinductionofEAUinCFA+R16+PTX-treated(CRP-treated)Fischer344rats.InvivoandinvitrodatademonstratedthatThl-cytokine,IFN-γmRNAexpressionwassignificantlyincreasedindiseasetargettissue-eyesandindraininglymphnodecellsofCRP-treatedFischer344rat.WhenIL-12andIFN-αmRNAexpressionwerecomparedintheexperimentalgroups,onlyIFN-αmRNAexpressionwasassociatedwithEAUdevelopment.TodistinguishthesourcesofIFN-αproducingcells,itwasobservedthatIFN-αexpressionwasmainlyproducedbymacrophages.ItwasfurtherconfirmedthatnormalmacrophagefromFischer344ratwasabletoproducesignificantIFN-αinthepresenceofPTX.ThedatastronglysuggestedthatIFN-αmightbeinvolvedininitiatingThl-celldifferentiationandinturncontributetotheinductionofEAU.HighIFN-αexpressioninducedbyPTXmayrepresentanovelpathwaytoinitiateThlresponseinFischer344rat.