Immunity拮抗性炎症表型决定肿
北京如何治疗白癜风 https://baike.baidu.com/item/%E5%8C%97%E4%BA%AC%E4%B8%AD%E7%A7%91%E7%99%BD%E7%99%9C%E9%A3%8E%E5%8C%BB%E9%99%A2/9728824
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01
AntagonisticInflammatoryPhenotypesDictateTumorFateandResponsetoImmuneCheckpointBlockade
Immunity
Inflammationcansupportorrestraincancerprogressionandtheresponsetotherapy.Bonavitaandcolleaguesextensivelycharacterizedthetumormicroenvironments(TME)ofhighlyTcell–inflamedtumors,thegrowthofwhichisrestrictedbytheimmunesysteminmice.Thisanalysisrevealedthatimmunecontrolofcyclooxygenase(COX)enzyme–deficienttumors,whicharedepletedoftheinflammation-associateddownstreamCOXproductprostaglandinE2(PGE2),dependedoninfiltrationbynaturalkiller(NK)cellsthatproduceIFNγ.TheseNKcellsnotonlykilledtumorcellseffectivelyontheirown,butalsocausedTMEremodelingthatledtoaccumulationofcytotoxicTcellsthatrestrictedtumorgrowth.TheeffectsofPGE2inthesetumorsweredeterminedtobemediatedbybindingofPGE2totheGprotein–coupledreceptorsEP2andEP4onNKcells,preventingNKcell–inducedTMEalterations,allowingtumorstocircumventimmunecontrol.Highlightingthepotentialclinicalrelevanceofthesefindings,aninvestigationofpatientdatasetsrepresentingavarietyofcancertypes,includingpatientsreceivingimmunecheckpointblockade(ICB)therapies,demonstratedthatthetypesofprotumorigenicandantitumorigenicTMEinflammatoryprofilesobservedinmicewerealsopresentinhumantumorsandwereprognosticallysignificantandpredictedresponseandsurvivalwithICB.Together,theseresultsrevealpreviouslyunknownmechanismsbywhichinflammation-associatedtumorcharacteristicsrelatetoimmunecontroloftumors,withclearimplicationsforICBefficacy.
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