NOD1 Cooperates with TLR2 to Enhance T Cell Receptor-Mediated Activation in CD8 T Cells 英文参考文献.docVIP
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NOD1 Cooperates with TLR2 to Enhance T Cell Receptor-Mediated Activation in CD8 T Cells 英文参考文献
NOD1CooperateswithTLR2toEnhanceTCellReceptor-
MediatedActivationinCD8TCells
BlandineC.Mercier1,2,3*,ErwanVentre1,2,3.,Marie-LaureFogeron1,2,3.,Anne-LaureDebaud1,2,3
MartineTomkowiak1,2,3,JacquelineMarvel1,2,3,NathalieBonnefoy1,2,3,4
,
*
1Universite′ deLyon,Lyon,France,2InstitutNationaldelaSante′ etdelaRechercheMe′dicale, U851,Lyon,France,3Universite′ Lyon1,Lyon,France,4HospicesCivilsde
Lyon,Lyon,France
Abstract
Patternrecognitionreceptors(PRR),likeToll-likereceptors(TLR)andNOD-likereceptors(NLR),areinvolvedinthedetection
of microbial infections and tissue damage by cells of the innate immune system. Recently, we and others have
demonstratedthatTLR2canadditionallyfunctionasacostimulatoryreceptoronCD8Tcells.Here,weestablishthatthe
intracytosolic receptor NOD1is expressed andfunctionalinCD8 Tcells. Weshowthat C12-iEDAP,asynthetic ligand for
NOD1,hasadirectimpactonbothmurineandhumanCD8Tcells,increasingproliferationandeffectorfunctionsofcells
activatedviatheirTcellreceptor(TCR).ThiseffectisdependentontheadaptormoleculeRIP2andisassociatedwithan
increasedactivationoftheNF-kB,JNKandp38signalingpathways.Furthermore,wedemonstratethatNOD1stimulation
cancooperatewithTLR2engagementonCD8TcellstoenhanceTCR-mediatedactivation.Altogetherourresultsindicate
thatNOD1mightfunctionasanalternativecostimulatoryreceptorinCD8Tcells.Ourstudyprovidesnewinsightsintothe
functionofNLRinTcellsandextendstoNOD1therecentconceptthatPRRstimulationcandirectlycontrolTcellfunctions.
Citation: Mercier BC, Ventre E, Fogeron M-L, Debaud A-L, Tomkowiak M, et al. (2012) NOD1 Cooperates with TLR2 to Enhance T Cell Receptor-Mediated
ActivationinCD8TCells.PLoSONE7(7):e42170.doi:10.1371/journal.pone.0042170
Editor:Jo¨rgHermannFritz,McGillUniversity,Canada
ReceivedDecember1,2011;AcceptedJuly3,2012;PublishedJuly27,2012
Copyright: ? 2012 Mercier et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricteduse,distribution,andreprodu
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