Toll-like receptors and their role in transplantation

被引:17
作者
Tesar, Bethany M. [1 ]
Goldstein, Daniel R. [1 ]
机构
[1] Yale Univ, Cardiol Sect, Dept Internal Med, New Haven, CT 06520 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
allograft; innate immunity; ischemia; mouse; MyD88; regulatory T cell; rejection; reperfusion; review; tolerance; Toll-like receptor; transplantation; xenograft;
D O I
10.2741/2382
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The innate immune system is an ancient, conserved pathogen response system that lays the foundation for self/non-self discrimination. The cells of the innate immune system are responsible for recognizing the highly conserved molecular motifs of microbial pathogens and represent the first line of immunological defense as well as contributing to the activation of the adaptive immune response. Toll-like receptors are a family of 13 germline-encoded receptors on antigen presenting cells, T cells and various non- lymphoid tissues that are critically important for innate immune function and inflammatory responses. Furthermore, numerous clinical and experimental animal studies have demonstrated the importance of Toll-like receptors as well as members of their signaling pathways in the setting of organ transplantation, where endogenous ligands may play a significant role. Toll- like receptor signaling has the capacity to inhibit transplantation tolerance. A complete understanding of the relationship between Toll- like receptor signaling and transplantation tolerance is essential to modifying, reducing or abrogating immune suppression as well as improving patient outcomes.
引用
收藏
页码:4221 / 4238
页数:18
相关论文
共 66 条
[1]   Heterologous immunity provides a potent barrier to transplantation tolerance [J].
Adams, AB ;
Williams, MA ;
Jones, TR ;
Shirasugi, N ;
Durham, MM ;
Kaech, SM ;
Wherry, EJ ;
Onami, T ;
Lanier, JG ;
Kokko, KE ;
Pearson, TC ;
Ahmed, R ;
Larsen, CP .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (12) :1887-1895
[2]   Mammalian Toll-like receptors [J].
Akira, S .
CURRENT OPINION IN IMMUNOLOGY, 2003, 15 (01) :5-11
[3]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[4]   Innate immunity and organ transplantation: The potential role of toll-like receptors [J].
Andrade, CF ;
Waddell, TK ;
Keshavjee, S ;
Liu, M .
AMERICAN JOURNAL OF TRANSPLANTATION, 2005, 5 (05) :969-975
[5]  
Bendigs S, 1999, EUR J IMMUNOL, V29, P1209, DOI 10.1002/(SICI)1521-4141(199904)29:04<1209::AID-IMMU1209>3.0.CO
[6]  
2-J
[7]   Genetic analysis of host resistance: Toll-like receptor signaling and immunity at large [J].
Beutler, Bruce ;
Jiang, Zhengfan ;
Georgel, Philippe ;
Crozat, Karine ;
Croker, Ben ;
Rutschmann, Sophie ;
Du, Xin ;
Hoebe, Kasper .
ANNUAL REVIEW OF IMMUNOLOGY, 2006, 24 :353-389
[8]   Toll-like receptor stimulation in cardiornyoctes decreases contractility and initiates an NF-κB dependent inflammatory response [J].
Boyd, John H. ;
Mathur, Sumeet ;
Wang, Yingjin ;
Bateman, Ryon M. ;
Walley, Keith R. .
CARDIOVASCULAR RESEARCH, 2006, 72 (03) :384-393
[9]   Regulatory T cells selectively express toll-like receptors and are activated by lipopolysaccharide [J].
Caramalho, I ;
Lopes-Carvalho, T ;
Ostler, D ;
Zelenay, S ;
Haury, M ;
Demengeot, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (04) :403-411
[10]   Direct stimulation of human T cells via TLR5 and TLR7/8:: Flagellin and R-848 up-regulate proliferation and IFN-γ production by memory CD4+ T cells [J].
Caron, G ;
Duluc, D ;
Frémaux, I ;
Jeannin, P ;
David, C ;
Gascan, H ;
Delneste, Y .
JOURNAL OF IMMUNOLOGY, 2005, 175 (03) :1551-1557