Innate immunity and organ transplantation: The potential role of toll-like receptors

被引:94
作者
Andrade, CF [1 ]
Waddell, TK [1 ]
Keshavjee, S [1 ]
Liu, M [1 ]
机构
[1] Univ Toronto, Dept Surg, Hlth Network, Toronto Gen Hosp,Thorac Surg Res Lab, Toronto, ON, Canada
关键词
adaptive immunity; 'danger signals'; ischemia-reperfusion; rejection;
D O I
10.1111/j.1600-6143.2005.00829.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
Traditionally, the recognition and tolerance of transplanted grafts has been considered to be within the realm of the adaptive immune system. Innate immunity, on the other hand, as the first line of host defense, plays a role in fighting against invading microorganisms. Recently, with the discovery of the Toll-like receptors (TLRs), the role of innate immune responses in the control of adaptive immunity has become a new area of interest. Emerging evidence suggests that in addition to responding to pathogen-associated molecular patterns of microorganisms, TLRs can be activated by endogenous ligands, expressed by mammalian cells. These ' danger signals ' may participate in ischemia-reperfusion related organ damage and subsequently influence function and survival of transplanted grafts. Furthermore, it has been suggested that adaptive immune responses can enhance the acute inflammatory responses controlled by innate immunity in organ transplantation. This review addresses the potential involvement of TLRs in different stages of organ transplantation. Intriguing and controversial findings are presented and discussed in order to stimulate more attention to this emerging and potentially important area of research in organ transplantation.
引用
收藏
页码:969 / 975
页数:7
相关论文
共 27 条
[1]  
ANDRADE C, 2004, AM J RESP CRIT CARE, V169, P203
[2]   Endogenous ligands of Toll-like receptors: implications for regulating inflammatory and immune responses [J].
Beg, AA .
TRENDS IN IMMUNOLOGY, 2002, 23 (11) :509-512
[3]   Dynamic changes in apoptotic and necrotic cell death correlate with severity of ischemia-reperfusion injury in lung transplantation [J].
Fischer, S ;
MacLean, AA ;
Liu, MY ;
Cardella, JA ;
Slutsky, AS ;
Suga, M ;
Moreira, JFM ;
Keshavjee, S .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2000, 162 (05) :1932-1939
[4]   Critical role of the Toll-like receptor signal adaptor protein MyD88 in acute allograft rejection [J].
Goldstein, DR ;
Tesar, BM ;
Akira, S ;
Lakkis, FG .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (10) :1571-1578
[5]   Analysis of differential immune responses induced by innate and adaptive immunity following transplantation [J].
He, HZ ;
Stone, JR ;
Perkins, DL .
IMMUNOLOGY, 2003, 109 (02) :185-196
[6]   Analysis of robust innate immune response after transplantation in the absence of adaptive immunity [J].
He, HZ ;
Stone, JR ;
Perkins, DL .
TRANSPLANTATION, 2002, 73 (06) :853-861
[7]   Toll-like receptor control of the adaptive immune responses [J].
Iwasaki, A ;
Medzhitov, R .
NATURE IMMUNOLOGY, 2004, 5 (10) :987-995
[8]   mRNA is an endogenous ligand for Toll-like receptor 3 [J].
Karikó, K ;
Ni, HP ;
Capodici, J ;
Lamphier, M ;
Weissman, D .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (13) :12542-12550
[9]   Postischemic reperfusion injury to allografts - A case for 'innate immunity'? [J].
Land, W .
EUROPEAN SURGICAL RESEARCH, 2002, 34 (1-2) :160-169
[10]   An essential role of the NF-κB/Toll-like receptor pathway in induction of inflammatory and tissue-repair gene expression by necrotic cells [J].
Li, M ;
Carpio, DF ;
Zheng, Y ;
Bruzzo, P ;
Singh, V ;
Ouaaz, F ;
Medzhitov, RM ;
Beg, AA .
JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7128-7135