Alpha-1,2-Mannosidase and Hence N-Glycosylation Are Required for Regulatory T Cell Migration and Allograft Tolerance in Mice 英文参考文献.docVIP

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Alpha-1,2-Mannosidase and Hence N-Glycosylation Are Required for Regulatory T Cell Migration and Allograft Tolerance in Mice 英文参考文献.doc

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Alpha-1,2-Mannosidase and Hence N-Glycosylation Are Required for Regulatory T Cell Migration and Allograft Tolerance in Mice 英文参考文献

Alpha-1,2-MannosidaseandHenceN-GlycosylationAre RequiredforRegulatoryTCellMigrationandAllograft ToleranceinMice ElaineT.Long*,StephanieBaker,VanessaOliveira¤a,BirgitSawitzki¤b,KathrynJ.Wood TransplantResearchImmunologyGroup,NuffieldDepartmentofSurgery,UniversityofOxford,JohnRadcliffeHospital,Oxford,UnitedKingdom Abstract Background: Specific immunological unresponsiveness to alloantigens can be induced in vivo by treating mice with a donoralloantigenincombinationwithanon-depletinganti-CD4antibody.Thistoleranceinductionprotocolenrichesfor alloantigenreactiveregulatoryTcells(Treg).Wepreviouslydemonstratedthatalpha-1,2-mannosidase,anenzymeinvolved in the synthesis and processing of N-linked glycoproteins, is highly expressed in tolerant mice, in both graft infiltrating leukocytesandperipheralbloodlymphocytes. PrincipalFindings:Inthisstudywehaveidentifiedthatalpha-1,2-mannosidaseexpressionincreasesinCD25+CD4+ Treg when they encounter alloantigen in vivo. Whenalpha-1,2-mannosidase enzymeactivity was blocked, Treg retained their capacitytosuppressTcellproliferationinvitrobutwereunabletobindtophysiologicallyrelevantligandsinvitro.Furtherin vivo analysis demonstrated that blocking alpha-1,2-mannosidase in Treg resulted in the migration of significantly lower numbers to the peripheral lymph nodes in skin grafted mice following adoptive transfer, where they were less able to inhibittheproliferation ofna?¨veTcellsrespondingtodonoralloantigen andhenceunablepreventallograftrejection in vivo. Significance:Takentogether,ourresultssuggestthatactivationofalloantigenreactiveTregresultsinincreasedalpha-1,2- mannosidase expression and altered N-glycosylation of cell surface proteins. In our experimental system, altered N- glycosylationisnotessentialforintrinsicTregsuppressivecapacity,butisessentialinvivoasitfacilitatesTregmigrationto sites where they can regulate immune priming. Migration of Treg is central to their role in regulating in vivo immune responsesandmayreq