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E3泛素连接酶BFAR调控TH9介导的抗肿瘤免疫反应的功能与作用机制研究.docx

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E3泛素连接酶BFAR调控TH9介导的抗肿瘤免疫反应的功能与作用机制研究 Title:FunctionandMechanismofE3UbiquitinLigaseBFARinRegulatingTH9-mediatedAnti-tumorImmuneResponse Introduction: Cancer,acomplexandheterogeneousdisease,continuestobeamajorglobalhealthchallenge.Immunotherapy,whichaimstoharnessthepoweroftheimmunesystemtofightagainstcancer,hasemergedasapromisingtreatmentstrategy.Thelper9(TH9)cells,asubsetofCD4+Tcells,haveshowngreatpotentialinpromotinganti-tumorimmuneresponses.However,theregulatorymechanismsunderlyingtheTH9-mediatedanti-tumorimmuneresponsearenotfullyunderstood.ThisstudyaimstoinvestigatethefunctionandmechanismofE3ubiquitinligaseBFARinregulatingtheTH9-mediatedanti-tumorimmuneresponse. FunctionofTH9cellsinanti-tumorimmunity: TH9cellsarecharacterizedbytheexpressionofIL-9,acytokinewithpleiotropiceffectsonbothimmuneandnon-immunecells.IL-9producedbyTH9cellspromotestherecruitmentandactivationofvariousimmunecells,includingnaturalkiller(NK)cells,dendriticcells(DCs),andcytotoxicCD8+Tcells.Additionally,IL-9enhancesthecytotoxicactivityoftheseimmunecells,ultimatelyleadingtotumorcelldeath.Furthermore,TH9cellsinducethedifferentiationoftumor-associatedmacrophagestowardsananti-tumorphenotype,furthercontributingtotheanti-tumorimmuneresponse. RoleofE3ubiquitinligaseBFARinTH9-mediatedanti-tumorimmuneresponse: E3ubiquitinligasesplaycriticalrolesinregulatingproteindegradationandcellularprocesses.BFAR,anE3ubiquitinligase,hasrecentlybeenimplicatedinimmuneregulation.SeveralstudieshavedemonstratedtheinvolvementofBFARinregulatingTcelldifferentiationandfunction.However,itsroleinTH9-mediatedanti-tumorimmunityremainslargelyunknown. MechanismsbywhichBFARregulatesTH9-mediatedanti-tumorimmuneresponse: 1.RegulationofTH9celldifferentiation:BFARmayinfluencethedifferentiationofnaiveCD4+TcellsintoTH9cellsbymodulatingtranscriptionfactorsinvolvedinTH9celldevelopment,suchasPU.1andIRF4.UnderstandinghowBFARinfluencesTH9celldifferentiationmayprovideinsightsintopotentialtherapeutictargetsforenhancingTH9-mediatedanti-tumorimmunere