Dendritic Cell-Mediated Regulation of Liver Ischemia-Reperfusion Injury and Liver Transplant Rejection.
Dendritic Cell-Mediated Regulation of Liver Ischemia-Reperfusion Injury and Liver Transplant Rejection.
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树突状细胞介导的肝缺血再灌注损伤和肝移植排斥反应的调控。
DOI：
10.3389/fimmu.2021.705465
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发表时间：
2021
影响因子：
7.3
通讯作者：
Thomson AW
中科院分区：
文献类型：
--
作者：
Nakano R;Tran LM;Geller DA;Macedo C;Metes DM;Thomson AW
Liver allograft recipients are more likely to develop transplantation tolerance than those that receive other types of organ graft. Experimental studies suggest that immune cells and other non-parenchymal cells in the unique liver microenvironment play critical roles in promoting liver tolerogenicity. Of these, liver interstitial dendritic cells (DCs) are heterogeneous, innate immune cells that appear to play pivotal roles in the instigation, integration and regulation of inflammatory responses after liver transplantation. Interstitial liver DCs (recruited in situ or derived from circulating precursors) have been implicated in regulation of both ischemia/reperfusion injury (IRI) and anti-donor immunity. Thus, livers transplanted from mice constitutively lacking DCs into syngeneic, wild-type recipients, display increased tissue injury, indicating a protective role of liver-resident donor DCs against transplant IRI. Also, donor DC depletion before transplant prevents mouse spontaneous liver allograft tolerance across major histocompatibility complex (MHC) barriers. On the other hand, mouse liver graft-infiltrating host DCs that acquire donor MHC antigen via “cross-dressing”, regulate anti-donor T cell reactivity in association with exhaustion of graft-infiltrating T cells and promote allograft tolerance. In an early phase clinical trial, infusion of donor-derived regulatory DCs (DCreg) before living donor liver transplantation can induce alterations in host T cell populations that may be conducive to attenuation of anti-donor immune reactivity. We discuss the role of DCs in regulation of warm and liver transplant IRI and the induction of liver allograft tolerance. We also address design of cell therapies using DCreg to reduce the immunosuppressive drug burden and promote clinical liver allograft tolerance.
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影响因子：
32.4
作者：
Dong, HD;Zhu, GF;Chen, LP
通讯作者：
Chen, LP
DOI：
10.1084/jem.20020045
发表时间：
2002-04-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Gilliet M;Boonstra A;Paturel C;Antonenko S;Xu XL;Trinchieri G;O'Garra A;Liu YJ
通讯作者：
Liu YJ
影响因子：
6.4
作者：
Collin M;Bigley V
通讯作者：
Bigley V
DOI：
10.4049/jimmunol.0900582
发表时间：
2009-12-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Castellaneta A;Sumpter TL;Chen L;Tokita D;Thomson AW
通讯作者：
Thomson AW
影响因子：
3.3
作者：
Chiang, YJ;Lu, L;Qian, SG
通讯作者：
Qian, SG