scholarly journals CD39 expression by hepatic myeloid dendritic cells attenuates inflammation in liver transplant ischemia-reperfusion injury in mice

Hepatology ◽  
2013 ◽  
Vol 58 (6) ◽  
pp. 2163-2175 ◽  
Author(s):  
Osamu Yoshida ◽  
Shoko Kimura ◽  
Edwin K. Jackson ◽  
Simon C. Robson ◽  
David A. Geller ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Liver Transplant ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myeloid Dendritic Cells

scholarly journals The Evolving Role of Neutrophils in Liver Transplant Ischemia-Reperfusion Injury

2019 ◽  
Vol 6 (1) ◽  
pp. 78-89 ◽  
Author(s):  
Kojiro Nakamura ◽  
Shoichi Kageyama ◽  
Jerzy W. Kupiec-Weglinski
Keyword(s):  
Liver Transplant ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Sphingosine 1-Phosphate Receptor 3–Deficient Dendritic Cells Modulate Splenic Responses to Ischemia-Reperfusion Injury

2015 ◽  
Vol 27 (4) ◽  
pp. 1076-1090 ◽  
Author(s):  
Amandeep Bajwa ◽  
Liping Huang ◽  
Elvira Kurmaeva ◽  
Joseph C. Gigliotti ◽  
Hong Ye ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sphingosine 1 Phosphate

F-37 Role of plasmacytoid dendritic cells in liver ischemia/reperfusion injury

2012 ◽  
Vol 44 ◽  
pp. S43
Author(s):  
A. Castellaneta ◽  
O. Yoshida ◽  
S. Kimura ◽  
N. Murase ◽  
M. Rendina ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Plasmacytoid Dendritic Cells ◽  
Liver Ischemia

Activated Renal Dendritic Cells Cross Present Intrarenal Antigens After Ischemia-Reperfusion Injury

2017 ◽  
Vol 101 (5) ◽  
pp. 1013-1024 ◽  
Author(s):  
Sarah L. Snelgrove ◽  
Cecilia Lo ◽  
Pam Hall ◽  
Camden Y. Lo ◽  
Maliha A. Alikhan ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

Abstract 99: Conditional Depletion of CD11c + Cells Attenuates Myocardial Ischemia-Reperfusion Injury in Mice

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Jun Li ◽  
Mozow Y Zuidema ◽  
Cuihua Zhang ◽  
Michael A. Hill ◽  
Feng Gao
Keyword(s):  
Dendritic Cells ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Diphtheria Toxin ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inflammatory Monocytes ◽  
Myocardial Ischemia Reperfusion ◽  
Inflammatory Macrophages

Excessive infiltration of pro-inflammatory monocytes /macrophages early after myocardial ischemia/reperfusion (MI/R) contributes to myocardial injury and cardiac dysfunction. We tested the hypothesis that conditional depletion of pro-inflammatory macrophages and dendritic cells may dampen excessive inflammatory response in the infarct myocardium, and thus attenuate MI/R injury. To achieve this, we took advantage of CD11c-diphtheria toxin receptor (DTR) transgenic mice, which allow for selective and conditional ablation of CD11c + cells for 2-3 days after diphtheria toxin administration. CD11c-DTR mice with conditional deficiency of CD11c + cells and wild type (WT) mice were subjected to MI/R (30 min /48 h). CD11c-DTR mice showed decreased infiltration of CD11c + dendritic cells and CD11c + F4/80 + macrophages in the I/R heart, reduced infarct size, attenuated myocardium apoptosis and improved cardiac function compared with those in WT mice. Moreover, inflammatory cytokines, such as TNF-α, MCP-1 and IFN-γ in the infracted myocardium as well as myocardial nitrotyrosine level, an index of oxidative and nitrative stresses, were dramatically decreased in CD11c-DTR mice than those in WT mice. These data indicate that the decreased infiltration of pro-inflammatory macrophages /dendritic cells and subsequent ameliorated inflammation may contribute to attenuated reperfusion injury and better reserved cardiac function in CD11c-DTR mice. This may provide potential novel strategies to target pro-inflammatory cells to reduce detrimental effects while sparing the beneficial wound healing roles of the recruited macrophages.

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