APC Activation Restores Functional CD4+CD25+ Regulatory T Cells in NOD Mice that Can Prevent Diabetes Development 英文参考文献.docVIP

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APC Activation Restores Functional CD4+CD25+ Regulatory T Cells in NOD Mice that Can Prevent Diabetes Development 英文参考文献.doc

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APCActivationRestoresFunctionalCD4CD25RegulatoryTCellsinNODMicethatCanPreventDiabetesDevelopment英文参考文献

APCActivationRestoresFunctionalCD4+CD25+ RegulatoryTCellsinNODMicethatCanPrevent DiabetesDevelopment JeanN.Manirarora1,2,MicheleM.Kosiewicz1,SarahA.Parnell1,PascaleAlard1* 1DepartmentofMicrobiologyandImmunology,UniversityofLouisville,HealthSciencesCenter(HSC),Louisville,Kentucky,UnitedStatesofAmerica,2Departmentof Pathology,St.JudeChildren’sResearchHospital,Memphis,Tennessee,UnitedStatesofAmerica Abstract Background:DefectsinAPCandregulatorycellsareassociatedwithdiabetesdevelopmentinNODmice.Wehaveshown previouslythatNODAPCarenoteffectiveatstimulatingCD4 CD25 regulatorycellfunctioninvitro.Wehypothesizethat + + + + failure of NOD APC to properly activate CD4 CD25 regulatory cells in vivo could compromise their ability to control pathogeniccells,andactivationofNODAPCcouldrestorethisdefect,therebypreventingdisease. Methodology/Principal Findings: To test these hypotheses, we used the well-documented ability of complete Freund’s adjuvant(CFA),anAPCactivator,topreventdiseaseinNODmice.PhenotypeandfunctionofCD4 CD25 regulatorycells + + fromuntreatedandCFA-treatedNODmiceweredeterminedbyFACS,andinvitroandinvivoassays.APCfromthesemice were also evaluated for their ability to activate regulatory cells in vitro. We have found that sick NOD CD4 CD25 cells expressedFoxp3atthesamepercentages,butdecreasedlevelspercell,comparedtoyoungNODornon-NODcontrols. + + TreatmentwithCFAincreasedFoxp3expressioninNODcells,andalsoincreasedthepercentagesofCD4 CD25 Foxp3+cells + + + + infiltratingthepancreascomparedtountreatedNODmice.Moreover,CD4 CD25 cellsfrompancreaticLNofCFA-treated, butnotuntreated,NODmicetransferredprotectionfromdiabetes.Finally,APCisolatedfromCFA-treatedmiceincreased Foxp3andgranzymeBexpressionaswellasregulatoryfunctionbyNODCD4 CD25 cellsinvitrocomparedtoAPCfrom + + untreatedNODmice. Conclusions/Significance:ThesedatasuggestthatregulatoryTcellfunctionandabilitytocontrolpathogeniccellscanbe enhancedinNODmicebyactivatingNODAPC. Citation: Manirarora