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，更多相关内容在学术论文-天天文库。
1、IFN-γdeficiencyexacerbatesexperimentalautoimmuneneuritisinmiceviaupregulatingTh17cellsdespiteamitigatedsystemicTh1immuneresponseHong-LiangZhang1,Xiang-YuZheng1,AzimullanSheikh2,Xiao-KeWang1,3,NaheedAmir2,RayomandPress4,AbduAdem2,JieZhu1,5,*1DepartmentofNeurobiology,CareSciencesandSoci
2、ety,KarolinskaInstitute,Stockholm,Sweden2DepartmentofPharmacology,FacultyofMedicineandHealthSciences,UnitedArabEmiratesUniversity,AlAin,UnitedArabEmirates3DepartmentofNeurosurgery,SecondHospitalofJilinUniversity,Changchun,China4DivisionofNeurology,DepartmentofClinicalNeuroscience,Karo
3、linskaInstitute,KarolinskaUniversityHospitalHuddinge,Stockholm,Sweden5DepartmentofNeurology,FirstHospitalofJilinUniversity,Changchun,China*Correspondingauthor:DrJieZhu,DepartmentofNeurobiology,CareSciencesandSociety,KarolinskaInstitute,KarolinskaUniversityHospitalHuddinge,Novum,plan5,
4、SE14186,Stockholm,Sweden(Tel.+46858585494;Fax.+46858585470;E-mail:Jie.Zhu@ki.se).30AbstractPreviousstudieshaveshownthatinterferon(IFN)-gisaproinflammatorycytokinethatcontributestothepathogenesisofGuillain-Barrésyndrome(GBS),aninflammatorydemyelinatingdiseaseoftheperipheralnervoussyste
5、m(PNS)inhumans,anditsanimalmodel,experimentalautoimmuneneuritis(EAN).Treatmentswithanti-IFN-gantibodiescanimproveclinicaloutcomeinGBSpatientsandEANanimals.AdministrationofIFN-gmarkedlyworsenedEAN.Paradoxically,themicedeficientinIFN-γremainsusceptibletoexperimentalautoimmuneencephalomy
6、elitis,ananalogousdiseaseinthecentralnervoussystem.TheseobservationsraiseaquestionwhetherIFN-γmightbeprotectiveinautoimmunedemyelinatingdiseases.ToclarifytheroleofIFN-ginthepathogenesisofautoimmunedemyelinatingdisease,weusedP0proteinpeptide180-199toinduceEANinIFN-gknockout(KO)mice.Aft
7、ertheacutephaseofEAN,theclinicalsignsofIFN-γKOmiceweresignificantlymoreseverethanthoseofwildtype(WT)controls.Afterantigenicstimulation,theproliferationofsplenicmononuclearcellwassignificantlyhigherinIFN-γKOthanWTmicewithEAN.AtthepeakofEAN,theproportionofinterleukin(IL)-17Aexpressingce
8、llsin
