Basal Activation of Type I Interferons (Alpha2 and Beta) and OAS Genes Insights into Differential Expression Profiles of Interferon System Components in Systemic Sclerosis英文文献资料.docVIP
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Basal Activation of Type I Interferons (Alpha2 and Beta) and OAS Genes Insights into Differential Expression Profiles of Interferon System Components in Systemic Sclerosis英文文献资料
HindawiPublishingCorporation
InternationalJournalofRheumatology
Volume2011,ArticleID275617,6pages
doi:10.1155/2011/275617
ResearchArticle
BasalActivationofTypeIInterferons(Alpha2andBeta)and
2
5
OASGenes:InsightsintoDifferentialExpressionPro?lesof
InterferonSystemComponentsinSystemicSclerosis
DaniloBretasdeOliveira,
Ant?onioCarlosMartinsGuedes,
ClaudioAnt?onioBonjardim, PauloC′esarPeregrinoFerreira,
1
GabrielMagnodeFreitasAlmeida,
2
1
Fl′aviaPatr′?ciaSenaTeixeiraSantos,
1
2
1
andErnaGeessienKroon
1
1
Laborat′oriodeV′?rus,InstitutodeCi?enciasBiol′ogicas,UniversidadeFederaldeMinasGerais,AvenueAnt?onioCarlos6627,
Pampulha31270-901BeloHorizonte,MG,Brazil
2
HospitaldasCl′?nicas,UniversidadeFederaldeMinasGerais,AvenueAlfredoBalena110,SantaE?g?enia,30130-100BeloHorizonte,
MG,Brazil
CorrespondenceshouldbeaddressedtoErnaGeessienKroon,kroone@icb.ufmg.br
Received15June2011;Revised10August2011;Accepted23August2011
AcademicEditor:LorindaChung
Copyright?2011DaniloBretasdeOliveiraetal. This is an open access article distributed under the Creative Commons
AttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkis
properlycited.
Objective.Systemicsclerosis(SSc)isacomplexautoimmunediseaseinwhichinterferons(IFNs)mayplayanessentialrole.We
hypothesizedthattypeIandIIIIFNsmaybefoundinincreasedlevelsinpatientsandberesponsibleforSScautoimmunestatus.
Methods.TypeIandIIIIFNandISGbasalexpressionpro?lesweremeasuredbyqPCRusingRNAfromPBMCsofpatientsand
controls.Results.TypeIIFNsareincreasedinSScpatients,whilenoinductionoftypeIIIIFNswasdetected.Thisinductioncannot
berelatedtoIRF7,sincenoupregulationofthisgenewasseenonpatients.OftheISGstested,25OASlevelswereincreasedin
patients,while6–16andMxAlevelswerenot.Conclusions.WhilethereisnoindicationoftypeIIIIFNinduction,increasedlevels
oftypeIIFNsmayleadtoabnormalregulationofISGsthatcanberesponsibleforimmunesystemalterationsdescribedforSSc.
1.Introduction
IFNs are immunomodulatory cytokine
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