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Enhanced FasL expression by HCV core...

University of Virginia.

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Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage./
作者:	Cruise, Michael Wayne.
面頁冊數:	248 p.
附註:	Adviser: Young S. Hahn.
Contained By:	Dissertation Abstracts International66-12B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3198444
ISBN:	9780542443558

Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage.
Cruise, Michael Wayne.

Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage. - 248 p.

Adviser: Young S. Hahn.

Thesis (Ph.D.)--University of Virginia, 2006.

Hepatitis C virus (HCV) infection is associated with a high rate of viral persistence and the development of chronic liver disease. Even though hepatocytes serve as a major reservoir for HCV infection, the virus can also infect PBMCs. The expression of HCV core protein in T cells can alter cell activation and is associated with liver inflammation. However, the molecular and cellular basis for the role of HCV core-expressing T cells in liver inflammation is not understood. Here, we use DO11.10 mice that express the HCV core protein in the OVA specific TCR on CD4+ T lymphocytes. In vivo antigenic stimulation triggers a marked influx of core-expressing antigen-specific CD4+ T cells into the liver of core(+)TCR mice but not their core(-)TCR littermates. This influx was accompanied by hepatic damage and elevations in serum ALT levels.

ISBN: 9780542443558Subjects--Topical Terms:

1017734
Biology, Microbiology.

Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage.
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245 1 0 $a Enhanced FasL expression by HCV core induces the production of CXCR3 chemokines and liver damage.
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500 $a Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6408.
502 $a Thesis (Ph.D.)--University of Virginia, 2006.
520 $a Hepatitis C virus (HCV) infection is associated with a high rate of viral persistence and the development of chronic liver disease. Even though hepatocytes serve as a major reservoir for HCV infection, the virus can also infect PBMCs. The expression of HCV core protein in T cells can alter cell activation and is associated with liver inflammation. However, the molecular and cellular basis for the role of HCV core-expressing T cells in liver inflammation is not understood. Here, we use DO11.10 mice that express the HCV core protein in the OVA specific TCR on CD4+ T lymphocytes. In vivo antigenic stimulation triggers a marked influx of core-expressing antigen-specific CD4+ T cells into the liver of core(+)TCR mice but not their core(-)TCR littermates. This influx was accompanied by hepatic damage and elevations in serum ALT levels.
520 $a Adoptive transfer of 111In-labeled CD4+ lymphocytes demonstrate that the core(+)TCR lymphocytes traffic primarily to the liver. Phenotypic analysis of the liver-infiltrating T cells revealed a highly activated phenotype with IHL from core(+)TCR mice demonstrating increased levels of FasL. Adoptive transfer of liver infiltrating core-expressing CD4 + T cells directly demonstrated the capacity of these activated T cells to induce liver inflammation. Importantly, anti-FasL antibody treatment of the mice abrogated the liver inflammation, suggesting that activated T cells expressing elevated levels of FasL may be involved in the bystander killing of hepatocyte, as well as the induction of chronic liver inflammation.
520 $a To understand the mechanism(s) of FasL-mediated liver inflammation, we examined the effect of FasL expressing CD4+ T cells on the initiation of hepatic damage through analysis of chemokine and chemokine receptor expression. Strikingly, liver inflammation in core(+)TCR mice was accompanied by a dramatic increase in IP-10 and Mig production. The intrahepatic lymphocytes were primarily CXCR3-positive and anti-CXCR3 antibody treatment abrogates migration of CXCR3+ lymphocytes into the liver and hepatic damage. Importantly, the blockade of Fas/FasL interaction reduces the expression of IP-10 and Mig and cellular infiltration into the liver. These findings suggest that activated CD4+ T cells with elevated FasL expression are involved in promoting liver inflammation and hepatic damage through the induction of chemokines.
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