<i>In situ</i> investigation of Fas/FasL expression in chronic hepatitis B infection and related liver diseases

Luo, Kun; Zhu, Yi; Zhang, L.-X.; He, Huaqiang; Wang, X.-S.; Zhang, L.

doi:10.1046/j.1365-2893.1997.00053.x

Cited by 49 publications

(38 citation statements)

References 8 publications

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“…The fragment intensity of FasL in rats with detectable FasL gene expression correlated with the fragment intensity of Fas. This is in agreement with studies of human hepatocellular carcinoma (20) and chronic hepatitis B infection (21) and the parallel increase in Fas and FasL in rats with LT could reflect increased apoptotic tissue destruction. The PCR technique does not allow the specific cell responsible for the Fas and FasL gene expression to be identified and we did not investigate characteristic morphological changes of apoptosis in the thyroids of BB/W rats.…”

Section: Discussionsupporting

confidence: 92%

Fas and Fas ligand gene expression in autoimmune thyroiditis in BB/W rats

Blüher

Krohn²,

Wallaschofski³

et al. 1999

European Journal of Endocrinology

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Objective: Apoptosis via the Fas pathway is a potential mechanism for thyroid tissue destruction leading to clinical hypothyroidism in Hashimoto's thyroiditis (HT). Recent studies reported contradictory results regarding the regulation of Fas/Fas ligand (FasL) expression by cytokines in vitro. We therefore determined the Fas and FasL gene expression in the BioBreeding/Worcester (BB/W) rat thyroiditis model, which can be regarded as a model for HT. Methods: In order to obtain BB/W rats with spontaneous, iodine-induced or without lymphocytic thyroiditis (LT), rats were divided into 3 groups: 55-day-old rats after 24 days of iodine administration, 75-day-old rats after 45 days of iodine administration, and 101-day-old rats respectively. The gene expression of Fas, FasL, and interleukin (IL)-1b was determined by Genescan fragment analysis using reverse polymerase chain reaction. Serum thyroglobulin (TG) antibody concentrations were measured and the extent of lymphocytic infiltration of one thyroid lobe was histologically graded. Results: Fas and FasL gene expression was significantly higher in rats with LT and correlated with the extent of lymphocytic infiltration and the TG antibody level. There was no evidence that the expression of IL-1b or other cytokines is related to the expression of Fas or its ligand. Conclusions:The increased expression of Fas and FasL in LT of BB/W rats suggests the involvement of the Fas pathway in the pathogenesis of LT in BB/W rats. However, in contrast to results of recent in vitro studies, in the BB/W rat Fas/FasL expression is not regulated by IL-2, -4, -6, -10, -12, interferon g, and tumor necrosis factor a.

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Section: Discussionsupporting

confidence: 92%

Fas and Fas ligand gene expression in autoimmune thyroiditis in BB/W rats

Blüher

Krohn²,

Wallaschofski³

et al. 1999

European Journal of Endocrinology

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“…In addition, signals released from these immune cells promote liver inflammation and chemotactically attract further inflammatory cells such as neutrophils (64). Several studies have shown that the elimination of virus-infected hepatocytes by cytotoxic T-cells mainly occurs via DRs, with Fas as the most prominent example (65,66). Increased Fas and FasL expression has actually been detected in virus-infected patients and correlates with severity and location of liver inflammation.…”

Section: B -Apoptosis In Viral Liver Diseasementioning

confidence: 99%

“…Increased Fas and FasL expression has actually been detected in virus-infected patients and correlates with severity and location of liver inflammation. Fas expression can be induced by both the expression of viral protein or inflammatory cytokines (65,66). Perhaps the two most important cytokines to this effect are interleukin-1 (IL-1), as generated early in the anti-viral response, and TNF-α, which acts as a pleiotropic late stage mediator (63,67).…”

Section: B -Apoptosis In Viral Liver Diseasementioning

confidence: 99%

Apoptosis in selected liver diseases

Kiliçarslan

Kahraman²,

Akkız³

et al. 2009

Turk J Gastroenterol

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“…[19][20][21] FasAg expression of hepatocytes is up-regulated in accordance with the severity of liver inflammation in chronic hepatitis C and B. 22,23 Elevated expression has also been reported in hepatitis B virus-related cirrhosis. 24 In addition, intrahepatic lymphocytes express FasL and show FasL-dependent cytolytic activity in patients with chronic hepatitis C. 21 However, little information was obtained about the role of the Fas system in the pathogenesis of recurrent HCV liver disease in patients who underwent OLT for HCV-related cirrhosis.…”

Section: H Epatitis C Virus (Hcv)-related Cirrhosis Currentlymentioning

confidence: 99%

Involvement of the Fas System in Hepatitis C Virus Recurrence After Liver Transplantation

Crespo¹

2000

Liver Transplantation

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To date, there have been no reports of the involvement of the Fas system in recurrent hepatitis C virus (HCV) infection after orthotopic liver transplantation (OLT). In 25 patients who underwent OLT for HCV-related liver cirrhosis, we evaluated the expression of the Fas antigen (FasAg) on hepatocytes, apoptic hepatocytes, and serum levels of soluble Fas (sFas). The level of HCV viremia and HCV genotype were determined by polymerase chain reaction. Serum sFas levels were determined by an enzyme immunoassay procedure. DNA fragmentation was determined by the terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate nick end-labeling (TUNEL) technique on deparaffinized liver samples. FasAg expression was evaluated by an immunoperoxidase method. Sixteen patients had evidence of recurrent HCV disease. The number of hepatocytes expressing FasAg and the percentage of apoptotic hepatocytes was greater among patients who developed recurrent hepatitis than among those who did not (P < .01 and P < .0001, respectively). There was a correlation between hepatic expression of FasAg, intensity of lobular inflammation (P ‫؍‬ .007), and TUNEL index (P < .001). The levels of sFas were greater among the patients with recurrent HCV hepatitis than those without recurrent hepatitis (P < .04). We conclude that (1) Fas expression is up-regulated in recurrent HCV after OLT and is related to the grading of liver disease; likewise, levels of sFas were greater in the patients with recurrent HCV hepatitis; and (2) the demonstration of hepatocytes with FasAg expression and the labeling of the nuclei by TUNEL assay suggest that hepatic apoptosis mediated by the Fas system may have a role in the pathogenesis of recurrent HCV hepatitis after OLT. (Liver Transpl 2000;6:562-569.) H epatitis C virus (HCV)-related cirrhosis currently accounts for approximately 25% to 40% of the indications for orthotopic liver transplantation (OLT). 1,2 Despite the nearly universal recurrence of HCV viremia, the degree to which recurrent hepatitis is recognized histologically varies markedly. [3][4][5][6] Factors that determine the frequency and severity of the disease have not been clearly identified, but a number of interrelated variables are probable, including level of HCV viremia, HCV genotype, and degree and type of immunosuppression. 2,3-6,7-9 However, the mechanism of liver cell damage in the patients with recurrent HCV liver disease is unknown.The apoptotic process, or programmed cell death, can be induced by stimuli of the so-called death receptors, such as the tumor necrosis factor (TNF) receptor-1, DR-3, DR-4, or Fas (APO-1, CD95). The Fas receptor or Fas antigen (FasAg) is a 45-kd cell-surface type 1 plasma membrane protein expressed in lymphoid and many other tissues. The receptor is activated through oligomerization on binding of its ligand (FasL) to its extracellular domain, and the apoptotic signal is transduced through the so-called death domain. [10][11][12] FasAg is one of the best-identified cell-surface molecules that mediate exter...

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In situ investigation of Fas/FasL expression in chronic hepatitis B infection and related liver diseases

Cited by 49 publications

References 8 publications

Fas and Fas ligand gene expression in autoimmune thyroiditis in BB/W rats

Fas and Fas ligand gene expression in autoimmune thyroiditis in BB/W rats

Apoptosis in selected liver diseases

Involvement of the Fas System in Hepatitis C Virus Recurrence After Liver Transplantation

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