Function of Fas/FasL and the mechanism of immune escape in the hepatoma cell line
Jiao Zhang
Abstract
Jiao Zhang
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.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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