Functional Status of Peripheral Blood T-Cells in Ischemic Stroke Patients 英文参考文献.docVIP

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Functional Status of Peripheral Blood T-Cells in Ischemic Stroke Patients 英文参考文献.doc

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Functional Status of Peripheral Blood T-Cells in Ischemic Stroke Patients 英文参考文献

FunctionalStatusofPeripheralBloodT-CellsinIschemic StrokePatients AntjeVogelgesang1.,VerenaE.L.May1.¤,UweGrunwald2,MarenBakkeboe1,SoenkeLangner3 ,Henry Wallaschofski4,ChristofKessler1,BarbaraM.Bro¨ker2,AlexanderDressel1* 1Department ofNeurology, University ofGreifswald,Greifswald, Germany, 2Institute for Immunology and Transfusion Medicine, University ofGreifswald,Greifswald, Germany,3DepartmentofRadiology,UniversityofGreifswald,Greifswald,Germany,4InstituteforClinicalChemistryandLaboratoryMedicine,UniversityofGreifswald, Greifswald,Germany Abstract Strokeisamajorcauseofdisabilityandleadingcauseofdeathinthenorthernhemisphere.Onlyrecentlyitbecameevident thatcerebralischemianotonlyleadstobraintissuedamageandsubsequentlocalinflammationbutalsotoadramaticloss ofperipheralbloodT-cellswithsubsequentinfections.However,onlyscarceinformationisavailableontheactivationstatus of surviving T cells. This study therefore addressed the functional consequences of immunological changes induced by stroke in humans. For this purpose peripheral blood T-cells were isolated from 93 stroke patients and the expression of activationmakerswasdetermined.InadditionexvivostimulationassayswereappliedtoassesthefunctionalityofTcells derivedfrombloodofstrokepatients.Comparedtohealthycontrols,strokepatientsdemonstratedanenhancedsurface expressionofHLA-DR(p,0.0001)andCD25(p=0.02)onTcells,revealingthatstrokeleadstoTcellactivation,whileCTLA-4 remainedundetectable. Invitrostudiesrevealedthat catecholaminesinhibit CTLA-4upregulation inactivated Tcells. Ex vivo,T cells of stroke patients proliferated unimpairedandreleased increased amounts of theproinflammatory cytokine TNF-a(p,0.01)andIL-6(p,0.05).Also,inseraofstrokepatientsHMGB1concentrationswereincreased(p=0.0002).The datademonstratethatsurvivingTcellsinstrokepatientsremainfullyfunctionalandareprimedtowardsaTH1response,in additionweprovideevidencethatcatecholaminemediatedinhibitionofCTLA-4expressionandserumHMGB1releaseare possiblemediatorsinstrokein