Administration of Mycobacterium leprae rHsp65 Aggravates Experimental Autoimmune Uveitis in Mice 英文参考文献.docVIP
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Administration of Mycobacterium leprae rHsp65 Aggravates Experimental Autoimmune Uveitis in Mice 英文参考文献
AdministrationofMycobacteriumlepraerHsp65
AggravatesExperimentalAutoimmuneUveitisinMice
ElianaB.Marengo1,3.,AlessandraGonc?alves Commodaro2.,JeanPierreS.Peron1,LucianaV.de
Moraes1,FernandaC.V.Portaro3,RubensBelfort,Jr.2,LuizVicenteRizzo4,OsvaldoAugustoSant’Anna3*
1DepartmentofImmunology,InstituteofBiomedicalSciences,UniversityofSa?o Paulo,Sa?o Paulo,Brazil,2VisionInstitute,FederalUniversityofSa?o Paulo,Sa?o Paulo,
Brazil,3ImmunochemistryLaboratory,InstitutoButantan,Sa?o Paulo,Brazil,4AlbertEinsteinJewishInstituteforEducationandResearch,Sa?o Paulo,Brazil
Abstract
The 60kDa heat shock protein family, Hsp60, constitutes an abundant and highly conserved class of molecules that are
highlyexpressedinchronic-inflammatoryandautoimmuneprocesses.Experimentalautoimmuneuveitis[EAU]isaTcell
mediatedintraocularinflammatorydiseasethatresembleshumanuveitis.MycobacterialandhomologousHsp60peptides
inducesuveitisinrats,howevertheirparticipationinaggravatingthediseaseispoorlyknown.Wehereevaluatetheeffects
oftheMycobacteriumlepraeHsp65inthedevelopment/progressionofEAUandtheautoimmuneresponseagainsttheeye
throughtheinductionoftheendogenousdisequilibriumbyenhancingtheentropyoftheimmunobiologicalsystemwith
theadditionofhomologousHsp.B10.RIIImicewereimmunizedsubcutaneouslywithinterphotoreceptorretinoid-binding
protein [IRBP], followed by intraperitoneally inoculation of M. leprae recombinant Hsp65 [rHsp65]. We evaluated the
proliferativeresponse,cytokineproductionandthepercentageofCD4 IL-17 ,CD4 IFN-c andCD4 Foxp3+cellsexvivo ,by
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flowcytometry.Diseaseseveritywasdeterminedbyeyehistologicalexaminationandserumlevelsofanti-IRBPandanti-
Hsp60/65measuredbyELISA.EAUscoresincreasedintheHsp65groupandwereassociatedwithanexpansionofCD4 IFN-
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c andCD4 IL-17 Tcells,corroboratingwithhigherlevelsofIFN-c.OurdataindicatethatrHsp65isoneofthemanagers
with a significant impact over the immune response during autoimmunity, skewing it to a pathogenic state, promot
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