Burn Injury Triggered Dysfunction in Dendritic Cell Response to TLR9 Activation and Resulted in Skewed T Cell Functions 英文参考文献.docVIP

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Burn Injury Triggered Dysfunction in Dendritic Cell Response to TLR9 Activation and Resulted in Skewed T Cell Functions 英文参考文献.doc

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Burn Injury Triggered Dysfunction in Dendritic Cell Response to TLR9 Activation and Resulted in Skewed T Cell Functions 英文参考文献

BurnInjuryTriggeredDysfunctioninDendriticCell ResponsetoTLR9ActivationandResultedinSkewedT CellFunctions HaitaoShen1,2,3,PatriciaE.deAlmeida1,KyungH.Kang1,PamelaYao2,CamieW.Chan1,2,4,5,6* 1Department of Cell Biology and Human Anatomy, University of California Davis, Davis, California, United States of America, 2Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, California, United States of America, 3Laboratory of Pathology, Hebei Medical University, Shijiazhuang,China,4StemCellRegenerativeMedicineConsortium,TheUniversityofHongKong,Pokfulam,HongKong,5DepartmentofAnatomy,TheUniversityof HongKong,Pokfulam,HongKong,6DepartmentofMedicine,TheUniversityofHongKong,Pokfulam,HongKong Abstract Severe trauma such as burn injury is often associated with a systemic inflammatory syndrome characterized by a hyperactive innate immune response and suppressed adaptive immune function. Dendritic cells (DCs), which sense pathogensviatheirToll-likereceptors(TLRs),playapivotalroleinprotectingthehostagainstinfections.Theeffectofburn injuryonTLR-mediatedDCfunctionisadebatedtopicandthemechanismcontrollingthepurportedimmunosuppressive response remains to be elucidated. Here we examined the effects of burn injury on splenic conventional DC (cDC) and plasmacytoidDC(pDC)responsestoTLR9activation.Wedemonstratethat,followingburntrauma,spleniccDCs’cytokine production profile in response to TLR9 activation became anti-inflammatory dominant, with high production of IL-10 (.50%increase)andlowproductionofIL-6,TNF-aandIL-12p70(,25–60%reduction).CD4+TcellsactivatedbythesecDCs weredefectiveinproducingTh1andTh17cytokines.Furthermore,burninjuryhadamoreaccentuatedeffectonpDCsthan on cDCs. Following TLR9 activation, pDCs displayed an immature phenotype with an impaired ability to secrete pro- inflammatory cytokines (IFN-a,IL-6 andTNF-a)and toactivate T cellproliferation. Moreover,cDCs andpDCs from burn- injured mice had low transcript levels of T