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1、Pleasecitethisarticleinpressas:Caietal.,PivotalRoleofDermalIL-17-ProducinggdTCellsinSkinInflammation,Immunity(2011),doi:10.1016/j.immuni.2011.08.001ImmunityArticlePivotalRoleofDermalIL-17-ProducinggdTCellsinSkinInflammationYihuaCai,1,2XiaoyanShen,1ChuanlinDing,2ChunjianQi,2KejiaLi,1XiaLi,1Venkatakrish
2、naR.Jala,2Huang-geZhang,2TianWang,3JieZheng,1,*andJunYan2,*1DepartmentofDermatology,RuijinHospital,SchoolofMedicine,ShanghaiJiaotongUniversity,Shanghai20025,P.R.China2DepartmentofMedicineandDepartmentofMicrobiologyandImmunology,JamesGrahamBrownCancerCenter,UniversityofLouisville,Louisville,KY40202,U
3、SA3DepartmentofMicrobiologyandImmunology,UniversityofTexasMedicalBranch,Galveston,TX77555,USA*Correspondence:jie-zheng2001@126.com(J.Z.),jun.yan@louisville.edu(J.Y.)DOI10.1016/j.immuni.2011.08.001SUMMARYaTh17cellcytokine,IL-22(Zhengetal.,2007),andthechemo-kinereceptorCCR6expressionisrequiredaswell(H
4、edricketal.,+Interleukin-23(IL-23)andCD4Thelper17(Th17)2009).TheimportanceofIL-23isfurtherdemonstratedbythecellsarethoughttobecriticalinpsoriasispathogen-therapeuticefficacyofhumanmAbagainstthesubunitofp40esis.Here,wereportthatIL-23predominantlystimu-ofIL-12andIL-23inthetreatmentofpsoriasis(Griffithse
5、tal.,lateddermalgdTcellstoproduceIL-17thatledto2010;Kruegeretal.,2007).IL-23-inducedskininflammationdiseaseprogression.DermalgdTcellsconstitutivelyhasprimarilybeenlinkedtothefunctionofTh17cellsandrelatedcytokines(DiCesareetal.,2009;Harperetal.,2009;Steinman,expressedtheIL-23receptor(IL-23R)andtranscr
6、ip-2010;Zabaetal.,2009).Therefore,IL-23andTh17cellsmaybetionalfactorRORgt.IL-17productionfromdermalgdkeymediatorsofdiseasepathogenesis(Blauvelt,2008).OneTcellswasindependentofabTcells.TheepidermalcaveatofthesestudiesisthatalthoughelevatedIL-17andhyperplasiaandinflammationinducedbyIL-23wereIL-22produc
7、tionisobservedinpsoriaticskin(Harperetal.,significantlydecreasedinTcellreceptord-deficient2009;Lowesetal.,2008;Wilsonetal.,2007;Zabaetal.,2007),//(Tcrd)andIL-17receptor-deficient(Il17ra)itisnotpresen