Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses 英文参考文献.docVIP

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Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses 英文参考文献.doc

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Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses 英文参考文献

DirectGeneTransferwithIP-10MutantAmeliorates MouseCVB3-InducedMyocarditisbyBluntingTh1 ImmuneResponses YanYue1,JunGui2,WenqingAi2,WeiXu2*,SidongXiong1,2* 1Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People’s Republic of China, 2Institute for Immunobiology,ShanghaiMedicalCollege,FudanUniversity,Shanghai,People’sRepublicofChina Abstract Background: Myocarditis is an inflammation of the myocardium that often follows the enterovirus infections, with coxsackievirus B3 (CVB3) being the most dominant etiologic agent. We and other groups previously reported that chemokineIP-10wassignificantlyinducedinthehearttissueofCVB3-infectedmiceandcontributedtothemigrationof massive inflammatory cells into the myocardium, which represents one of the most important mechanisms of viral myocarditis. To evaluate the direct effect of IP-10 on the inflammatory responses in CVB3 myocarditis, herein an IP-10 mutantdeprivedofchemo-attractantfunctionwasintroducedintomicetoantagonizetheendogenousIP-10activity,and itstherapeuticeffectonCVB3-inducedmyocarditiswasevaluated. Methodology/PrincipalFindings:ThedepletionmutantpIP-10-AT,withanadditionalmethionineafterremovalofthe5N- terminal amino acids, was genetically constructed and intramuscularly injected into BALB/c mice after CVB3 infection. Comparedwithvectorornotreatment,pIP-10-ATtreatmenthadsignificantlyreducedheart/bodyweightratioandserum CK-MB level, increased survival rate and improved heart histopathology, suggesting an ameliorated myocarditis. This therapeuticeffectwasnotattributabletoanenhancedviralclearance,buttoabluntedTh1immuneresponse,asevidenced + + + bysignificantlydecreasedsplenicCD4 /CD8 IFN-c TcellpercentagesandreducedmyocardialTh1cytokinelevels. Conclusion/Significance: Our findings constitute the first preclinical data indicating that interfering in vivo IP-10 activity couldameliorateCVB3inducedmyocarditis.Thisstrategy mayrepresentasanewtherapeutic appro