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1、在小鼠骨髓移植中CCR5与急性移植物抗宿主病的相关性研究论文【摘要】本研究评价供者CCR5在经过强化预处理的骨髓移植动物模型受者体内的作用，为今后的异基因造血干细胞移植的临床应用提供科学依据。经过致死剂量照射的BALB/c小鼠接受异基因C57BL/6小鼠的骨髓移植。根据回输的细胞不同实验分为4组：B6CCR5KO组，受者接受C57BL/6CCR5-/-小鼠骨髓和脾脏细胞；B6C组，受者只接受C57BL/6CCR5-/-小鼠骨髓细胞；B6C组，受者只接受野生型C57BL/6小鼠骨髓细胞。结果表明：较之B6Tasselves),recruitothercells
2、inthegenerationoforgandamage［1,2］.Thisinpartisthe“cytokinestorm”thatfuelsGVHDpathogenesis［3］.MultipleorgansareaffectedinacuteGVHDincludingtheskin,gut,lungs,andliver.TcontributestothegenerationandpathologyofGVHDinbothmanandmouse［4,5］,emphasizingtheimportanceofmodelsthatcanreflectthe
3、conditioningregimensusedinclinicalBMT.Chemokinesareadiversegroupofcytokinesthatmodulateimmunecelltraffickingandfunction［6,7］.Duetothepropertiesofchemokines,.freelokinesmayplayaroleinGVHD.Serodyetal［8］demonstratedreducedlethalityinrecipientsofdonorTcellsfromMIP-1α-deficientmicepared
4、toediatedGVHDmodel.RecentreportsalsoindicatedthatblockadeofCCR5usingneutralizingantibodiescouldalsoprotectfromGVHDusingaparentintoF1GVHDmodel［9］.ThisreportandanotherusingCCR5KOmiceinthesamemodelindicatedthatCCR5oncellsplayedaroleinaugmentingtheGVHDresponseandthatblockadeofthisinter
5、actioncouldbeusedtopreventGVHD［9,10］.Hoechanismunderlyingthisprotectionayplayaroleindoeinfectiousdiseasemodels［11］,suggestingthatthisreceptor-ligandinteractionmayexertdiverseeffects.ThepreviousreportsassessingtheroleofCCR5expressiononGVHDusedamodelininistered.Chemokineproductionasa
6、rkedlyinfluencedbyinflammatorycytokinesinducedaftertotal-bodyirradiation(TBI)［12,13］.T.OurresultsdemonstratethattheabsenceofCCR5ondonorcellsresultsinasignificantincreaseinGVHDmorbiditythattheAnimalProductionArea(NCIatFrederick,Frederick,MD,USA).C57BL/6CCR5-/-mice(B6CCR5KO)tKuziel.A
7、llrecipientsatchedfemalesandonthsofageatthetimeofBMT.CellpreparationBonemarrothebackbones,femurs,andtibiaeintoDulbecco′sphosphate-bufferedsalinesolution(DPBS)ortarandpestle,filteringthroughameshfiltertoremoveparticulates,andphnodecellpreparationsovedebrisandented(FBS)forinvitroassa
8、ys.CellcountsedonaCoulterZ
