Quetiapine, an Atypical Antipsychotic, Is Protective against Autoimmune-Mediated Demyelination by Inhibiting Effector T Cell Proliferation 英文参考文献.docVIP

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Quetiapine, an Atypical Antipsychotic, Is Protective against Autoimmune-Mediated Demyelination by Inhibiting Effector T Cell Proliferation 英文参考文献.doc

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Quetiapine, an Atypical Antipsychotic, Is Protective against Autoimmune-Mediated Demyelination by Inhibiting Effector T Cell Proliferation 英文参考文献

Quetiapine,anAtypicalAntipsychotic,IsProtective againstAutoimmune-MediatedDemyelinationby InhibitingEffectorTCellProliferation FengMei1.,ShengGuo2.,YangtaoHe1,LinyunWang1,HongkaiWang1,JianqinNiu1,JimingKong3, XinminLi4,YuzhangWu2,LanXiao1* 1Department of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China, 2Department of Immunology, Third Military Medical University, Chongqing, China, 3Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada, 4DepartmentofPsychiatry,UniversityofManitoba,Winnipeg,Canada Abstract Quetiapine (Que), a commonly used atypical antipsychotic drug (APD), can prevent myelin from breakdown without immune attack. Multiple sclerosisis (MS), an autoimmune reactive inflammation demyelinating disease, is triggered by activatedmyelin-specificTlymphocytes(Tcells).Inthisstudy,weinvestigatedthepotentialefficacyofQueasanimmune- modulating therapeutic agent for experimental autoimmune encephalomyelitis (EAE), a mouse model for MS. Que treatmentwasinitiatedontheonsetofMOG35–55 peptideinducedEAEmiceandtheefficacyofQueonmodulatingthe + + immuneresponsewasdeterminedbyFlowCytometrythroughanalyzingCD4 /CD8 populationsandtheproliferationof + effectorTcells(CD4 CD252)inperipheralimmuneorgans.OurresultsshowthatQuedramaticallyattenuatestheseverityof + + EAEsymptoms.QuetreatmentdecreasestheextentofCD4 /CD8 Tcellinfiltrationintothespinalcordandsuppresseslocal glialactivation,therebydiminishingthelossofmatureoligodendrocytesandmyelinbreakdowninthespinalcordofEAE + + mice.OurresultsfurtherdemonstratethatQuetreatmentdecreasestheCD4 /CD8 Tcellpopulationsinlymphnodesand spleensofEAEmiceandinhibitseitherMOG35–55 oranti-CD3inducedproliferationaswellasIL-2productionofeffectorT + cells (CD4 CD252) isolated from EAE mice spleen. Together, these findings suggest that Que displays an immune- modulatingroleduringthecourseofEAE,andthusmaybeapromisingcandidatefor