Expression of Fas antigen in liver tissue of patients with chronic hepatitis B and C

Öksüz, Murat; Akkız, Hikmet; Yf, Isiksal; Şeydaoğlu, Gülşah; Serin, Mehmet Sami; Kayaselçuk, Fazi̇let; Abaylı, Bahri; Tuncer, İlyas

doi:10.1097/00042737-200403000-00015

Cited by 12 publications

(8 citation statements)

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“…Briefly, apoptotic bodies characterized by nuclear and cell fragmentation within the shrunken and condensed cytoplasm were found, and there were a number of cells, consisting of spindle-shaped activated Kupffer cells, mononuclear cells and neutrophils, in the sinusoid. Such findings have often been observed in human patients with liver injuries as the apopto-necro-inflammatory reaction [33,36].…”

Section: Liver Histopathology After Hb-egf or Hgf Gene Therapymentioning

confidence: 62%

“…Recent studies have suggested that the initial and essential event in acute and/or chronic hepatitis, including fulminant hepatic failure, may be the excessive activation of the Fas system [33,34] and that the administration of the agonistic anti-Fas antibody in mice leads to fulminant hepatic failure [14,35]. As we clearly elucidated the therapeutic effect of HGF in this animal model [14], this model may be suitable to use for the initial examination of the in vivo anti-apoptotic effect on hepatocytes and the therapeutic potential of a certain agent for liver disorders.…”

Section: Liver Enzymes After Hb-egf or Hgf Gene Therapymentioning

confidence: 99%

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In vivo hepatic HB-EGF gene transduction inhibits Fas-induced liver injury and induces liver regeneration in mice: A comparative study to HGF

Khai¹,

Takahashi²,

Ushikoshi³

et al. 2006

Journal of Hepatology

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Section: Liver Histopathology After Hb-egf or Hgf Gene Therapymentioning

confidence: 62%

Section: Liver Enzymes After Hb-egf or Hgf Gene Therapymentioning

confidence: 99%

In vivo hepatic HB-EGF gene transduction inhibits Fas-induced liver injury and induces liver regeneration in mice: A comparative study to HGF

Khai¹,

Takahashi²,

Ushikoshi³

et al. 2006

Journal of Hepatology

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“…Fas expression was obviously increased on hepatocytes in the HBs-Tg mice compared with the C57BL/6 mice ( Figures 3b and c ), which caused the hepatocytes to be more sensitive to NKT cell-mediated cytotoxicity through Fas/FasL signaling after CpG triggering ( Figure 4 ). Enhanced Fas expression in liver tissues has also been observed in patients with HBV- or hepatitis C virus-associated chronic liver diseases, 37 , 38 and there was a progressive increase in its expression with the severity of the liver disease. Moreover, augmentation of the Fas system has been implicated in the pathogenesis of alcoholic liver disease, autoimmune hepatitis and biliary disorders.…”

Section: Discussionmentioning

confidence: 87%

CD205-TLR9-IL-12 axis contributes to CpG-induced oversensitive liver injury in HBsAg transgenic mice by promoting the interaction of NKT cells with Kupffer cells

et al. 2016

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Gut-derived bacterial products contribute to liver inflammation and injury during chronic hepatitis B virus infection; however, the underlying mechanisms remain obscure. In this study, hepatitis B surface antigen transgenic (HBs-Tg) mice and their wild-type (WT) control C57BL/6 mice were injected with CpG-oligodeoxynucleotides (ODNs) to mimic the translocation of gut microbial products into the systemic circulation. We found that, compared with the WT mice, the HBs-Tg mice were oversensitive to CpG-ODN-induced liver injury, which was dependent on natural killer T (NKT) cells. CpG-ODN injection enhanced the expression of Fas ligand (FasL) on NKT cells. In addition, hepatocytes from the HBs-Tg mice expressed higher levels of Fas than did those from the WT mice, which was further augmented by CpG-ODN. Interaction of Fas and FasL was involved in the cytotoxicity of NKT cells against hepatocytes in the HBs-Tg mice. Moreover, Kupffer cells in the HBs-Tg mice expressed higher levels of CD205 and produced greater amounts of interleukin (IL)-12 than did those in the WT mice. Finally, the depletion of Kupffer cells, neutralization of IL-12 or specific silencing of CD205 on Kupffer cells significantly inhibited CpG-ODN-induced liver injury and NKT activation in the HBs-Tg mice. Our data suggest that CD205-expressing Kupffer cells respond to CpG-ODNs and subsequently release IL-12 to promote NKT cell activation. Activated NKT cells induce liver damage through the Fas signaling pathway in HBs-Tg mice.

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“…Studies underline the role of the Fas/FasL pathway in the immuneinduced pathogenesis by the killing of noninfected cells (bystander cells) [81,83]. Interestingly, while normal liver does not express Fas, in chronic hepatitis C, the expression of Fas is upregulated in hepatocytes [84,85]. Bantel et al describe the correlation between the degree of inflammation of the liver and the number of apoptotic cells as measured by detection of activated caspases, including caspase-3, a hallmark of FasFasL activation [86].…”

Section: Cd8þ T-cell Response: Negative Sidementioning

confidence: 99%

Hepatitis C virus and the immune system: a concise review

Gremion

Cerny

2005

Reviews in Medical Virology

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Hepatitis C Virus (HCV) induces a chronic infection in 50%-80% of infected individuals, which can lead to cirrhosis and hepatocellular carcinoma. The inefficiency of the immune system in eliminating the virus is not well understood as humoral and cellular immune responses are induced. While a persistent infection is generally associated with a weak CD4+ and CD8+ T cell response during the acute phase, there is no good explanation as to why this response is strong enough in 20% of acutely infected people such that they spontaneously resolve the infection. However, the immune system partially controls the viral infection but due to a long-lasting inflammatory milieu, hepatic damage occurs. During the chronic phase of the infection, HCV does not seem to be cytopathic. This aspect is still controversial as the virus was linked to the development of cholestatic syndrome or acute lobular hepatitis after liver transplant in HCV infected patients. The development of new experimental systems such as HCV pseudoparticles, genomic replicon and transfected cell lines have improved our vision of the virus cycle as well as the understanding of the mechanism of persistence. However, a convincing explanation for the chronicity of the infection in the presence of a functional immune response is still missing and is an important area of research to understand HCV immune pathogenesis. Future research should dissect mechanisms that lead to quantitatively or qualitatively inadequate immune responses, the role of the high variability of the virus, the relevance of host's genetic factors and mechanisms of immunosuppression induced by the virus.

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Expression of Fas antigen in liver tissue of patients with chronic hepatitis B and C

Abstract: These findings suggest that apoptosis of hepatocytes is induced via the Fas antigen and contributes to the elimination of infected cells.

Cited by 12 publications

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In vivo hepatic HB-EGF gene transduction inhibits Fas-induced liver injury and induces liver regeneration in mice: A comparative study to HGF

In vivo hepatic HB-EGF gene transduction inhibits Fas-induced liver injury and induces liver regeneration in mice: A comparative study to HGF

CD205-TLR9-IL-12 axis contributes to CpG-induced oversensitive liver injury in HBsAg transgenic mice by promoting the interaction of NKT cells with Kupffer cells

Hepatitis C virus and the immune system: a concise review

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