Protein synthesis of the pro-inflammatory S100A8A9 complex in plasmacytoid dendritic cells and cell surface S100A8A9 on leukocyte subpopulations in systemic lupus erythematosus 英文参考文献.docVIP

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Protein synthesis of the pro-inflammatory S100A8A9 complex in plasmacytoid dendritic cells and cell surface S100A8A9 on leukocyte subpopulations in systemic lupus erythematosus 英文参考文献.doc

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Protein synthesis of the pro-inflammatory S100A8A9 complex in plasmacytoid dendritic cells and cell surface S100A8A9 on leukocyte subpopulations in systemic lupus erythematosus 英文参考文献

Loodetal.ArthritisResearchTherapy2011,13:R60 /content/13/2/R60 RESEARCH ARTICLE OpenAccess Proteinsynthesisofthepro-inflammatory S100A8/A9complexinplasmacytoiddendritic cellsandcellsurfaceS100A8/A9onleukocyte subpopulationsinsystemiclupuserythematosus ChristianLood1,2*,MartinStenstr?m3,HelenaTydén2,BirgittaGullstrand1,EvaK?llberg3,TomasLeanderson3, LennartTruedsson1,GunnarSturfelt2,FredrikIvars3andAndersABengtsson2 Abstract Introduction:Systemiclupuserythematosus(SLE)isanautoimmunediseasewithchronicorepisodic inflammationinmanydifferentorgansystems,activationofleukocytesandproductionofpro-inflammatory cytokines.Theheterodimerofthecytosoliccalcium-bindingproteinsS100A8andS100A9(S100A8/A9)issecreted byactivatedpolymorphonuclearneutrophils(PMNs)andmonocytesandservesasaserummarkerforseveral inflammatorydiseases.Furthermore,S100A8andS100A9havemanypro-inflammatorypropertiessuchasbinding toToll-likereceptor4(TLR4).InthisstudyweinvestigatedifaberrantcellsurfaceS100A8/A9couldbeseeninSLE andifplasmacytoiddendriticcells(pDCs)couldsynthesizeS100A8/A9. Methods:Flowcytometry,confocalmicroscopyandreal-timePCRofflowcytometry-sortedcellswereusedto measurecellsurfaceS100A8/A9,intracellularS100A8/A9andmRNAlevelsofS100A8andS100A9,respectively. Results:CellsurfaceS100A8/A9wasdetectedonallleukocytesubpopulationsinvestigatedexceptforTcells.By confocalmicroscopy,real-timePCRandstimulationassays,wecoulddemonstratethatpDCs,monocytesandPMNs couldsynthesizeS100A8/A9.Furthermore,pDCcellsurfaceS100A8/A9washigherinpatientswithactivediseaseas comparedtopatientswithinactivedisease.Uponimmunecomplexstimulation,pDCsup-regulatedthecellsurface S100A8/A9.SLEpatientshadalsoincreasedserumlevelsofS100A8/A9. Conclusions:PatientswithSLEhadincreasedcellsurfaceS100A8/A9,whichcouldbeimportantinamplification andpersistenceofinflammation.Importantly,pDCswereabletosynthesizeS100A8/A9proteinsandup-regulate thecellsurfaceexpressionuponimmunecomplex-stimulation.Thus,S100A8/A9maybeapotenttargetfor treatmentofinflam