fax: 585-273-2452
1527-3350/asset/olbannerleft.gif?v=1&s=4b2409f9534ed500d3c8da1940a23842e2b9932d)
1527-3350/asset/olbannerright.gif?v=1&s=141b9a8485298533c3e2016e937b0404f7d933e1)
Original Article
You have full text access to this OnlineOpen article
Immune role of hepatic TLR-4 revealed by orthotopic mouse liver transplantation†
Article first published online: 22 DEC 2006
DOI: 10.1002/hep.21446
Copyright © 2006 American Association for the Study of Liver Diseases
Additional Information
How to Cite
John, B., Klein, I. and Crispe, I. N. (2007), Immune role of hepatic TLR-4 revealed by orthotopic mouse liver transplantation. Hepatology, 45: 178–186. doi: 10.1002/hep.21446
- †
Potential conflict of interest: Nothing to report.
- ‡
fax: 585-273-2452
Publication History
- Issue published online: 22 DEC 2006
- Article first published online: 22 DEC 2006
- Manuscript Accepted: 6 SEP 2006
- Manuscript Received: 5 JUL 2006
Funded by
- NIH. Grant Number: RO1AI063353
- DFG. Grant Number: KL140/2-1
- Abstract
- Article
- References
- Cited By
Abstract
Activated CD8+ T cells migrate to the liver at the end of an immune response and go through apoptosis there, but this mechanism is impaired in mice lacking Toll-like receptor-4. This allowed us to test the importance of liver trapping in an ongoing immune response. In the absence of Toll-like receptor-4, reduced liver accumulation was associated with an increase in the circulating CD8+ T cell pool, more long-lived memory T cells and increased CD8+ T cell memory responses. Using experimental orthotopic liver transplantation, we showed that the effect of Toll-like receptor-4 on the formation of the CD8+ T cell memory resides in the liver. Conclusion: These studies reveal a new function for the liver, which is to regulate the magnitude of T cell memory responses through a Toll-like receptor-4–dependent mechanism. (HEPATOLOGY 2007;45:178–186.)