2006Journal of Shandong UniversityRequires access

Function of Fas/FasL and the mechanism of immune escape in the hepatoma cell line

Jiao Zhang

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Abstract

Objective: To investigate the mechanism of immune escape through Fas/FasL pathway in hepatoma cells.Methods: Fas and FasL expressions of hepatoma cell line HepG2.2.15 were examined by flow cytometry.Resistance of hepatoma cells to Fas-mediated apoptosis was determined by using anti-Fas agonistic monoclonal antibody CH11.FasL function of inducing T-lymphocytes to apoptosis was assessed by coculture assays in vitro by using hepatoma cells HepG2.2.15 and Jurkat cells.Results: ①Fas expression of HepG2.2.15 was low,and CH11 could not induce the cells to apoptosis;②FasL expression rate of HepG2.2.15 was 18.03%,and FasL could induce Jurkat cells to apoptosis in coculture assays;③The apoptosis rate of Jurkat cells in coculture assays was decreased from 21.41% to 8.91% after FasL having been blocked with FasL-neutralizing antibody NOK-2. Conclusions: Hepatoma cells can resist to Fas-mediated apoptosis,and FasL expressed by the cells can inhibit the immune function of T-lymphocytes.Fas/FasL pathway is one of the mechanisms of immune escape in hepatoma cells and may be a new target point of immunological therapy.

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Objective: To investigate the mechanism of immune escape through Fas/FasL pathway in hepatoma cells.Methods: Fas and FasL expressions of hepatoma cell line HepG2.2.15 were examined by flow cytometry.Resistance of hepatoma cells to Fas-mediated apoptosis was determined by using anti-Fas agonistic monoclonal antibody CH11.FasL function of inducing T-lymphocytes to apoptosis was assessed by coculture assays in vitro by using hepatoma cells HepG2.2.15 and Jurkat cells.Results: ①Fas expression of HepG2.2.15 was low,and CH11 could not induce the cells to apoptosis;②FasL expression rate of HepG2.2.15 was 18.03%,and FasL could induce Jurkat cells to apoptosis in coculture assays;③The apoptosis rate of Jurkat cells in coculture assays was decreased from 21.41% to 8.91% after FasL having been blocked with FasL-neutralizing antibody NOK-2. Conclusions: Hepatoma cells can resist to Fas-mediated apoptosis,and FasL expressed by the cells can inhibit the immune function of T-lymphocytes.Fas/FasL pathway is one of the mechanisms of immune escape in hepatoma cells and may be a new target point of immunological therapy.

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Available abstract

Objective: To investigate the mechanism of immune escape through Fas/FasL pathway in hepatoma cells.Methods: Fas and FasL expressions of hepatoma cell line HepG2.2.15 were examined by flow cytometry.Resistance of hepatoma cells to Fas-mediated apoptosis was determined by using anti-Fas agonistic monoclonal antibody CH11.FasL function of inducing T-lymphocytes to apoptosis was assessed by coculture assays in vitro by using hepatoma cells HepG2.2.15 and Jurkat cells.Results: ①Fas expression of HepG2.2.15 was low,and CH11 could not induce the cells to apoptosis;②FasL expression rate of HepG2.2.15 was 18.03%,and FasL could induce Jurkat cells to apoptosis in coculture assays;③The apoptosis rate of Jurkat cells in coculture assays was decreased from 21.41% to 8.91% after FasL having been blocked with FasL-neutralizing antibody NOK-2. Conclusions: Hepatoma cells can resist to Fas-mediated apoptosis,and FasL expressed by the cells can inhibit the immune function of T-lymphocytes.Fas/FasL pathway is one of the mechanisms of immune escape in hepatoma cells and may be a new target point of immunological therapy.

Key concepts: Fas ligand, Jurkat cells, Apoptosis, Immune system, Cell biology, Flow cytometry, Biology, Fas receptor

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