资源描述：
《删除干扰素gamma对实验性自身免疫性神经炎的作用》由会员上传分享，免费在线阅读，更多相关内容在行业资料-天天文库。
1、IFN-γdeficiencyexacerbatesexperimentalautoimmuneneuritisinmiceviaupregulatingTh17cellsdespiteamitigatedsystemicTh1immuneresponseHong-LiangZhang1,Xiang-YuZheng1,AzimullanSheikh2,Xiao-KeWang1,3,NaheedAmir2,RayomandPress4,AbduAdem2,JieZhu1,5,*1DepartmentofNeurobiology,CareSciencesand
2、Society,KarolinskaInstitute,Stockholm,Sweden2DepartmentofPharmacology,FacultyofMedicineandHealthSciences,UnitedArabEmiratesUniversity,AlAin,UnitedArabEmirates3DepartmentofNeurosurgery,SecondHospitalofJilinUniversity,Changchun,China4DivisionofNeurology,DepartmentofClinicalNeuroscie
3、nce,KarolinskaInstitute,KarolinskaUniversityHospitalHuddinge,Stockholm,Sweden5DepartmentofNeurology,FirstHospitalofJilinUniversity,Changchun,China*Correspondingauthor:DrJieZhu,DepartmentofNeurobiology,CareSciencesandSociety,KarolinskaInstitute,KarolinskaUniversityHospitalHuddinge,
4、Novum,plan5,SE14186,Stockholm,Sweden(Tel.+46858585494;Fax.+46858585470;E-mail:Jie.Zhu@ki.se).30AbstractPreviousstudieshaveshownthatinterferon(IFN)-gisaproinflammatorycytokinethatcontributestothepathogenesisofGuillain-Barrésyndrome(GBS),aninflammatorydemyelinatingdiseaseoftheperiph
5、eralnervoussystem(PNS)inhumans,anditsanimalmodel,experimentalautoimmuneneuritis(EAN).Treatmentswithanti-IFN-gantibodiescanimproveclinicaloutcomeinGBSpatientsandEANanimals.AdministrationofIFN-gmarkedlyworsenedEAN.Paradoxically,themicedeficientinIFN-γremainsusceptibletoexperimentala
6、utoimmuneencephalomyelitis,ananalogousdiseaseinthecentralnervoussystem.TheseobservationsraiseaquestionwhetherIFN-γmightbeprotectiveinautoimmunedemyelinatingdiseases.ToclarifytheroleofIFN-ginthepathogenesisofautoimmunedemyelinatingdisease,weusedP0proteinpeptide180-199toinduceEANinI
7、FN-gknockout(KO)mice.AftertheacutephaseofEAN,theclinicalsignsofIFN-γKOmiceweresignificantlymoreseverethanthoseofwildtype(WT)controls.Afterantigenicstimulation,theproliferationofsplenicmononuclearcellwassignificantlyhigherinIFN-γKOthanWTmicewithEAN.AtthepeakofEAN,theproportionofint
8、erleukin(IL)-17Aexpressingcellsin
