The role of HMGB1 in heart transplantation

被引:9
|
作者
Lv, Qianying [1 ]
Li, Chao [2 ]
Mo, Yarui [3 ]
He, Long [1 ,4 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Wuhan Childrens Hosp, Dept Nephrol, Wuhan 430016, Peoples R China
[2] Peking Union Med Coll, China & Japan Friendship Hosp, Dept Emergency, Beijing 10073, Peoples R China
[3] Peking Union Med Coll, Union Hosp, Dept Pediat, Beijing 10032, Peoples R China
[4] Huazhong Univ Sci & Technol, Puai Hosp, Tongji Med Coll, Dept Clin Lab, Wuhan 430033, Hubei, Peoples R China
关键词
Heart transplantation; HMGB1; Ischemia-reperfusion injury; Acute rejection; Chronic rejection; Xenogenic rejection; GLYCATION END-PRODUCTS; MOBILITY GROUP BOX-1; LUNG TRANSPLANTATION; COLD ISCHEMIA/REPERFUSION; CARDIAC TRANSPLANTATION; INTERNATIONAL SOCIETY; ALLOGRAFT-REJECTION; DENDRITIC CELLS; MECHANISMS; IMMUNITY;
D O I
10.1016/j.imlet.2017.11.014
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
There has been significant progress in the field of heart transplantation over the last 45 years. Although the role of adaptive immunity in heart allograft rejection has been extensively studied for decades, there is increasing evidence that suggests that the innate immune system also contributes to the development of heart allograft rejection. The high-mobility group box (HMGB) proteins, particularly HMGB1, are self-derived innate immune activators that have multiple functions in the regulation of immunity and inflammation. Recent discoveries have illustrated the close link between HMGB1 and heart allograft rejection. In this review, we summarize current knowledge of the function of HMGB1 as a ligand that can evoke inflammatory responses and ultimately cause rejection after heart transplantation.
引用
收藏
页码:1 / 3
页数:3
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