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Considering Liver Transplant

Considering Liver Transplant? These two articles may give you some understanding as to why the new liver graft or liver may become re-infected after surgery and what is in the research to prevent re-infection. It is an interesting read in that it may be the beginning of new treatments many years a head. The Adaptive Immunotherapy was posted by board member “Trish” and the subsequent article was a follow up of that article as to why the virus may flourish.

 

Adoptive immunotherapy with liver allograft–derived lymphocytes induces anti-HCV activity after liver transplantation in humans and humanized mice

http://www.jci.org/articles/view/38374

 

After liver transplantation in HCV-infected patients, the virus load inevitably exceeds pre-transplantation levels. This phenomenon reflects suppression of the host-effector immune responses that control HCV replication by the immunosuppressive drugs used to prevent rejection of the transplanted liver. Here, we describe an adoptive immunotherapy approach, using lymphocytes extracted from liver allograft perfusate (termed herein liver allograft–derived lymphocytes), which includes an abundance of NK/NKT cells that mounted an anti-HCV response in HCV-infected liver transplantation recipients, despite the immunosuppressive environment. This therapy involved intravenously injecting patients 3 days after liver transplantation with liver allograft–derived lymphocytes treated with IL-2 and the CD3-specific mAb OKT3. During the first month after liver transplantation, the HCV RNA titers in the sera of recipients who received immunotherapy were markedly lower than those in the sera of recipients who did not receive immunotherapy. We further explored these observations in human hepatocyte–chimeric mice, in which mouse hepatocytes were replaced by human hepatocytes. These mice unfailingly developed HCV infections after inoculation with HCV-infected human serum. However, injection of human liver–derived lymphocytes treated with IL-2/OKT3 completely prevented HCV infection. Furthermore, an in vitro study using genomic HCV replicon–containing hepatic cells revealed that IFN-γ–secreting cells played a pivotal role in such anti-HCV responses. Thus, our study presents what we believe to be a novel paradigm for the inhibition of HCV replication in HCV-infected liver transplantation recipients.

 

Costimulatory molecule programmed death-1 in the cytotoxic response during chronic hepatitis C

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773891/

 

Hepatitis C virus (HCV)-specific CD8+ T cells play an important role in the resolution of HCV infection. Nevertheless, during chronic hepatitis C these cells lack their effector functions and fail to control the virus. HCV has developed several mechanisms to escape immune control.

 

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Start Date
Feb 08, 2010
by jepperone
Last Revision
Feb 08, 2010
by jepperone
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