AIM: To investigate the mechanism of alpha-fetoprotein (AFP) in escaping from the host immune surveillance of hepatocellular carcinoma. METHODS: AFP purified from human umbilical blood was administrated into the cultured human lymphoma Jurkat T cell line or hepatoma cell line, Bel7402 in vitro. The expression of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) and its receptor (TRAILR) mRNA were analyzed by Northern blot and Western blot was used to detect the expression of Fas and Fas ligand (FasL) protein. RESULTS: AFP (20 mg/L) could promote the expression of FasL and TRAIL, and inhibit the expression of Fas and TRAILR of Bel7402 cells. For Jurkat cell line, AFP could suppress the expression of FasL and TRAIL, and stimulate the expression of Fas and TRAILR. AFP also could synergize with Bel7402 cells to inhibit the expression of FasL protein and TRAIL mRNA in Jurkat cells. The monoclonal antibody against AFP (anti-AFP) could abolish these functions of AFP. CONCLUSION: AFP is able to promote the expression of FasL and TRAIL in hepatoma cells and enhance the expression of Fas and TRAILR in lymphocytes. These could elicit the escape of hepatocellular carcinoma cells from the host's lymphocytes immune surveillance.
AIM: To investigate the mechanism of alpha-fetoprotein (AFP) in escaping from the host immune surveillance of hepatocellular carcinoma. METHODS:AFP purified from human umbilical blood was administrated into the cultured humanlymphoma Jurkat T cell line or hepatoma cell line, Bel7402 in vitro. The expression of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) and its receptor (TRAILR) mRNA were analyzed by Northern blot and Western blot was used to detect the expression of Fas and Fas ligand (FasL) protein. RESULTS:AFP (20 mg/L) could promote the expression of FasL and TRAIL, and inhibit the expression of Fas and TRAILR of Bel7402 cells. For Jurkat cell line, AFP could suppress the expression of FasL and TRAIL, and stimulate the expression of Fas and TRAILR. AFP also could synergize with Bel7402 cells to inhibit the expression of FasL protein and TRAIL mRNA in Jurkat cells. The monoclonal antibody against AFP (anti-AFP) could abolish these functions of AFP. CONCLUSION:AFP is able to promote the expression of FasL and TRAIL in hepatoma cells and enhance the expression of Fas and TRAILR in lymphocytes. These could elicit the escape of hepatocellular carcinoma cells from the host's lymphocytes immune surveillance.
Authors: Stephen A Renshaw; Jasvir S Parmar; Vanessa Singleton; Sarah J Rowe; David H Dockrell; Steven K Dower; Colin D Bingle; Edwin R Chilvers; Moira K B Whyte Journal: J Immunol Date: 2003-01-15 Impact factor: 5.422
Authors: M Irmler; M Thome; M Hahne; P Schneider; K Hofmann; V Steiner; J L Bodmer; M Schröter; K Burns; C Mattmann; D Rimoldi; L E French; J Tschopp Journal: Nature Date: 1997-07-10 Impact factor: 49.962
Authors: Philippe Gabant; Lesley Forrester; Jennifer Nichols; Thierry Van Reeth; Christelle De Mees; Bernard Pajack; Alistair Watt; Johan Smitz; Henri Alexandre; Claude Szpirer; Josiane Szpirer Journal: Proc Natl Acad Sci U S A Date: 2002-09-24 Impact factor: 11.205
Authors: Cornelius Schmaltz; Onder Alpdogan; Barry J Kappel; Stephanie J Muriglan; Jimmy A Rotolo; Jennifer Ongchin; Lucy M Willis; Andrew S Greenberg; Jeffrey M Eng; James M Crawford; George F Murphy; Hideo Yagita; Henning Walczak; Jacques J Peschon; Marcel R M van den Brink Journal: Nat Med Date: 2002-11-11 Impact factor: 53.440
Authors: Pavel Taimr; Hajime Higuchi; Eva Kocova; Richard A Rippe; Scott Friedman; Gregory J Gores Journal: Hepatology Date: 2003-01 Impact factor: 17.425