Innate immunity and organ transplantation: focus on lung transplantation

被引:53
作者
Kreisel, Daniel [1 ,2 ,3 ]
Goldstein, Daniel R. [4 ,5 ]
机构
[1] Washington Univ, Dept Surg, St Louis, MO USA
[2] Washington Univ, Dept Pathol, St Louis, MO 63130 USA
[3] Washington Univ, Dept Immunol, St Louis, MO 63130 USA
[4] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA
[5] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA
关键词
immunobiology; organ transplantation; TOLL-LIKE RECEPTOR; ISCHEMIA-REPERFUSION INJURY; BRONCHIOLITIS OBLITERANS SYNDROME; ACUTE ALLOGRAFT-REJECTION; VERSUS-HOST-DISEASE; PHASE PROTEIN HAPTOGLOBIN; SIGNAL ADAPTER PROTEIN; ISCHEMIA/REPERFUSION INJURY; INFLAMMATORY RESPONSE; ALVEOLAR MACROPHAGE;
D O I
10.1111/j.1432-2277.2012.01549.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
Ischemia reperfusion injury (IRI) that occurs with solid organ transplantation activates the innate immune system to induce inflammation. This leads to enhanced acute allograft rejection, impaired transplant tolerance and accelerated progression of chronic rejection. In this review, we discuss the innate immune signaling pathways that have been shown to play a role in organ transplantation. In particular, we focus on Toll-like receptor signaling pathways and how they have influenced outcomes after organ transplantation both experimentally and from clinical studies. Furthermore, we describe the substances that trigger the innate immune system after transplantation and several of the key cellular mediators of inflammation. We specifically point out unique aspects of activation of the innate immune system after lung transplantation. Finally, we discuss the areas that should be investigated in the future to more clearly understand the influence of the innate immune system after organ transplantation.
引用
收藏
页码:2 / 10
页数:9
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