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InfarctedMyocardium-PrimedDendriticCellsImproveRemodelingandCardiacFunctionAfterMyocardialInfarctionbyModulatingtheRegulatoryTCellandMacrophagePolarizationEunHoChoo,Jun-HoLee,Eun-HyePark,etal.
Circulation,.
Preventionofpostinfarctventricularremodelingisanunmetclinicalneed.Inflammatoryresponsesplayacriticalroleinleftventricularremodelingaftermyocardialinfarction(MI).Tolerogenicdendriticcells(tDCs)canmodulateimmuneresponses,inducingregulatoryTcellsinanumberofinflammatorydiseases.Inthisstudy,theauthorsprovidedthattDCtherapyinapreclinicalmodelofMIwaspotentiallytranslatableintoananti-remodelingtherapyforischemictissuerepair.TheyfoundthatinvivocardiacmagneticresonanceimagingandexvivohistologyconfirmedthebeneficialeffectonpostinfarctleftventricularremodelinginMImicetreatedwithtDCs.Subcutaneouslyadministeredinfarctlysate–primedtDCsneartheinguinallymphnodemigratedtotheregionallymphnodeandinducedinfarcttissue–specificregulatoryT-cellpopulationsintheinguinalandmediastinallymphnodes,spleen,andinfarctedmyocardium,indicatingthatalocalinjectionoftDCsinducesasystemicactivationofMI-specificregulatoryTcells.Also,theycanleadtoanearlymacrophagesubsetshiftfrominflammatoryM1toreparativeM2macrophages.Thealteredimmuneenvironmentintheinfarctedheartresultedinabetterwoundremodeling,preservedleftventricularsystolicfunctionaftermyocardialtissuedamage,andimprovedsurvival.