Opposing Roles for Interferon Regulatory Factor-3 (IRF-3) and Type I Interferon Signaling during Plague 英文参考文献.docVIP

下载本文档

3
0
约7.16万字
约 15页
2017-05-12 发布于上海
举报
版权申诉

Opposing Roles for Interferon Regulatory Factor-3 (IRF-3) and Type I Interferon Signaling during Plague 英文参考文献.doc

1、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。。
2、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
4、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
5、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
6、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
7、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Opposing Roles for Interferon Regulatory Factor-3 (IRF-3) and Type I Interferon Signaling during Plague 英文参考文献

OpposingRolesforInterferonRegulatoryFactor-3(IRF-3) andTypeIInterferonSignalingduringPlague AmiA.Patel1,2,HanniLee-Lewis1,2,JenniferHughes-Hanks1.,CraigA.Lewis3.,DeborahM.Anderson1,2 * 1DepartmentofVeterinaryPathobiology,UniversityofMissouri,Columbia,Missouri,UnitedStatesofAmerica,2LaboratoryforInfectiousDiseaseResearch,Universityof Missouri,Columbia,Missouri,UnitedStatesofAmerica,3StarlingEnterprise,LLC,Columbia,Missouri,UnitedStatesofAmerica Abstract Type I interferons (IFN-I) broadly control innate immunity and are typically transcriptionally induced by Interferon RegulatoryFactors(IRFs)followingstimulationofpatternrecognitionreceptorswithinthecytosolofhostcells.Forbacterial infection,IFN-Isignalingcanresultinwidelyvariantresponses,insomecasescontributingtothepathogenesisofdisease whileinotherscontributingtohostdefense.Inthiswork,weaddressedtheroleoftypeIIFNduringYersiniapestisinfection in a murine model of septicemic plague. Transcription of IFN-b was induced in vitro and in vivo and contributed to pathogenesis.MicelackingtheIFN-Ireceptor,Ifnar,werelesssensitivetodiseaseandharboredmoreneutrophilsinthelater stage of infection which correlated with protection from lethality. In contrast, IRF-3, a transcription factor commonly involvedininducingIFN-bfollowingbacterialinfection,wasnotnecessaryforIFNproductionbutinsteadcontributedto hostdefense.Invitro,phagocytosisofY.pestisbymacrophagesandneutrophilswasmoreeffectiveinthepresenceofIRF-3 andwasnotaffectedbyIFN-bsignaling.ThisactivitycorrelatedwithlimitedbacterialgrowthinvivointhepresenceofIRF- 3.TogetherthedatademonstratethatIRF-3isabletoactivatepathwaysofinnateimmunityagainstbacterialinfectionthat extendbeyondregulationofIFN-bproduction. Citation:PatelAA,Lee-LewisH,Hughes-HanksJ,LewisCA,AndersonDM(2012)OpposingRolesforInterferonRegulatoryFactor-3(IRF-3)andTypeIInterferon SignalingduringPlague.PLoSPathog8(7):e1002817.doi:10.1371/journal.ppat.1002817 Editor:RalphR.Isberg,TuftsUniversitySchoolofMedicine,UnitedStatesof