Enhanced Th17-Cell Responses Render CCR2-Deficient Mice More Susceptible for Autoimmune Arthritis 英文参考文献.docVIP

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Enhanced Th17-Cell Responses Render CCR2-Deficient Mice More Susceptible for Autoimmune Arthritis 英文参考文献.doc

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Enhanced Th17-Cell Responses Render CCR2-Deficient Mice More Susceptible for Autoimmune Arthritis 英文参考文献

EnhancedTh17-CellResponsesRenderCCR2-Deficient MiceMoreSusceptibleforAutoimmuneArthritis RishiR.Rampersad1,TeresaK.Tarrant1,ChristopherT.Vallanat1,TatianaQuintero-Matthews1, MichaelF.Weeks1,DeniseA.Esserman2,3,JenniferClark3,FrancoDiPadova4,DhavalkumarD.Patel1,4, AlanM.Fong1,PengLiu1* 1DepartmentofMedicine,ThurstonArthritisResearchCenter,UniversityofNorthCarolinaatChapelHill,ChapelHill,NorthCarolina,UnitedStatesofAmerica,2Division ofGeneralMedicineandClinicalEpidemiology,DepartmentofMedicine,UniversityofNorthCarolinaatChapelHill,ChapelHill,NorthCarolina,UnitedStatesofAmerica, 3Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 4Novartis Institutes for BioMedical Research,Basel,Switzerland Abstract CCR2isconsideredaproinflammatorymediatorinmanyinflammatorydiseasessuchasrheumatoidarthritis.However,mice lacking CCR2 develop exacerbated collagen-induced arthritis. To explore the underlying mechanism, we investigated whether autoimmune-associated Th17 cells were involved in the pathogenesis of the severe phenotype of autoimmune arthritis.WefoundthatTh17cellswereexpandedapproximately3-foldinthedraininglymphnodesofimmunizedCCR22/2 micecomparedtoWTcontrols(p=0.017),whereasthenumberofTh1cellsandregulatoryTcellsaresimilarbetweenthese twogroupsofmice.Consistently,levelsoftheTh17cellcytokineIL-17AandTh17cell-associatedcytokines,IL-6andIL-1b were approximately 2–6-fold elevated in the serum and 22–28-fold increased in the arthritic joints in CCR22/2 mice comparedtoWTmice(p=0.04,0.0004,and0.01forIL-17,IL-6,andIL-1b,respectively,intheserumandp=0.009,0.02,and 0.02inthejoints).Furthermore,typeIIcollagen-specificantibodiesweresignificantlyincreased,whichwasaccompaniedby B cell and neutrophil expansion in CCR22/2 mice. Finally, treatment with an anti-IL-17A antibody modestly reduced the diseaseseverityinCCR22/2mice.Therefore,weconcludethatwhilewedetectmarkedlyenhancedTh17-cellresponsesin collagen-inducedar