Soluble MOG35-55I-Ab Dimers Ameliorate Experimental Autoimmune Encephalomyelitis by Reducing Encephalitogenic T Cells 英文参考文献.docVIP

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Soluble MOG35-55I-Ab Dimers Ameliorate Experimental Autoimmune Encephalomyelitis by Reducing Encephalitogenic T Cells 英文参考文献.doc

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Soluble MOG35-55I-Ab Dimers Ameliorate Experimental Autoimmune Encephalomyelitis by Reducing Encephalitogenic T Cells 英文参考文献

SolubleMOG35-55/I-AbDimersAmeliorateExperimental AutoimmuneEncephalomyelitisbyReducing EncephalitogenicTCells YeliGong,ZhigangWang,ZhihuiLiang,HongxiaDuan,LichenOuyang,QianYu,ZheXu,GuanxinShen, XiufangWeng*,XiongwenWu* DepartmentofImmunology,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,Wuhan,China Abstract The MOG35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice is a useful animal model to explore therapeutic approaches to T cell-mediated autoimmune diseases because the dominant T-cell epitope(s)havebeendefined.Itisrationalthatantigen-specificimmunosuppressioncanbeinducedbyusingMHC-peptide complexesasspecificTCRligand(s)thatinteractwithautoreactiveTcellsintheabsenceofco-stimulation.Inthisstudy, a soluble divalent MOG35-55/I-Ab fusion protein (MOG35-55/I-Ab dimer) was constructed to specifically target the + autoreactiveCD4 TcellsintheEAEmouse.IntraperitonealadministrationoftheMOG35-55/I-Abdimersignificantlydelayed andamelioratedEAEsymptomsbyreducingEAE-relatedinflammationinthemouseCNSandreducingencephalitogenic Th1andTh17cellsintheperipherallymphoidorgans.Weobservedthatdimerinterventionataconcentrationof1.2nM suppressedMOG35-55peptide-specific2D2transgenicTcells(2D2Tcells)proliferationbyover90%afterinvitroactivation withMOG35-55peptide.Themechanismsinvolvedinthisantigen-specificdimer-mediatedsuppressionwerefoundtobe downregulated TCR-CD3 expression as well as upregulated expression of membrane-bound TGF-b (mTGF-b) and IL-10 + suppressivecytokinesbytheautoreactiveCD4 Tcells.Collectively,ourdatademonstratesthatsolubledivalentMHCclassII molecules can abrogate pathogenic T cells in EAE. Furthermore, our data suggests that this strategy may provide an efficientandclinicallyusefuloptiontotreatautoimmunediseases. Citation:GongY,WangZ,LiangZ,DuanH,OuyangL,etal.(2012)SolubleMOG35-55/I-AbDimersAmeliorateExperimentalAutoimmuneEncephalomyelitisby ReducingEncephalitogenicTCells.PLoSONE7(10):e47435.doi:10.1371/journal