BACKGROUND/AIMS: Human intrahepatic biliary epithelial cells can express immune recognition elements and are targets for immune attack in several liver pathologies. The aim of this study was to investigate the ability of biliary epithelial cells to act as accessory cells for T cell activation in normal and inflammatory conditions. METHODS: Normal biliary epithelial cells were cocultured with allogeneic unstimulated and mitogen- or antigen-stimulated peripheral blood lymphocytes. T cell responses were assessed by flow cytometry. RESULTS: Biliary epithelial cells did not induce allostimulation in resting T cells and inhibited T cell activation in response to either phytohaemagglutinin, mitogenic anti-CD3 antibody or recall antigen, irrespective of the presence of accessory cells. Biliary epithelial cells did not affect T cell viability, promote or inhibit activation-induced apoptosis nor modulate expression of CD95/Fas. In presence of biliary epithelial cells, stimulated T cells failed to develop an antigen-committed (CD45R0hi) phenotype and were unresponsive to subsequent CD3 ligation. However, T cells underwent normal activation in the presence of biliary epithelial cells which had been pre-treated with Interferon gamma or TGFbeta, cytokines implicated in liver disease. CONCLUSIONS: In normal liver, biliary epithelial cells inhibit rather than promote T cell activation, but their anergising effects may be overcome in response to trauma.
BACKGROUND/AIMS: Human intrahepatic biliary epithelial cells can express immune recognition elements and are targets for immune attack in several liver pathologies. The aim of this study was to investigate the ability of biliary epithelial cells to act as accessory cells for T cell activation in normal and inflammatory conditions. METHODS: Normal biliary epithelial cells were cocultured with allogeneic unstimulated and mitogen- or antigen-stimulated peripheral blood lymphocytes. T cell responses were assessed by flow cytometry. RESULTS: Biliary epithelial cells did not induce allostimulation in resting T cells and inhibited T cell activation in response to either phytohaemagglutinin, mitogenic anti-CD3 antibody or recall antigen, irrespective of the presence of accessory cells. Biliary epithelial cells did not affect T cell viability, promote or inhibit activation-induced apoptosis nor modulate expression of CD95/Fas. In presence of biliary epithelial cells, stimulated T cells failed to develop an antigen-committed (CD45R0hi) phenotype and were unresponsive to subsequent CD3 ligation. However, T cells underwent normal activation in the presence of biliary epithelial cells which had been pre-treated with Interferon gamma or TGFbeta, cytokines implicated in liver disease. CONCLUSIONS: In normal liver, biliary epithelial cells inhibit rather than promote T cell activation, but their anergising effects may be overcome in response to trauma.
Authors: Jorge Allina; Bin Hu; Daniel M Sullivan; Maria Isabel Fiel; Swan N Thung; Steven F Bronk; Robert C Huebert; Judy van de Water; Nicholas F LaRusso; M E Gershwin; Gregory J Gores; Joseph A Odin Journal: J Autoimmun Date: 2007-01-10 Impact factor: 7.094
Authors: Yasunori Ichiki; Carlo Selmi; Shinji Shimoda; Hiromi Ishibashi; Stuart C Gordon; M Eric Gershwin Journal: Clin Rev Allergy Immunol Date: 2005-04 Impact factor: 8.667
Authors: Magdalena Molero-Abraham; Jose L Sanchez-Trincado; Marta Gomez-Perosanz; Alvaro Torres-Gomez; Jose Luis Subiza; Esther M Lafuente; Pedro A Reche Journal: Front Immunol Date: 2019-06-28 Impact factor: 7.561