Published online Jul 14, 2005. doi: 10.3748/wjg.v11.i26.4090
Revised: December 12, 2004
Accepted: December 16, 2004
Published online: July 14, 2005
AIM: To explore a novel mechanism for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), upregulation of CD4+ and CD8+ T lymphocytes participating in the patho-physiological process of chronic hepatitis B (CHB).
METHODS: The levels of serum soluble TRAIL (sTRAIL), serum IFN-γ and membrane-bound TRAIL expression on peripheral leucocytes from 58 CHB patients were examined by ELISA and flow cytometry respectively. The levels of TRAIL were compared with the baseline levels of 17 healthy controls, and correlation analysis was performed between ALT, TBIL, PT, morphological change in hepatic tissues, and serum IFN-γ.
RESULTS: The results showed that TRAIL levels on membranes of CD4+, CD8+ T cells in CHB patients were much higher than those in healthy controls (P < 0.001), and were correlated with serum TBIL (r = 0.354, P = 0.008 for CD4+ and r = 0.522, P = 0.000 for CD8+, respectively), ALT (r = 0.393, P = 0.003 for CD8+), PT (r = 0.385,P = 0.004 for CD8+) and serum IFN-γ level (r = 0.302, P = 0.011 for CD4+ and r = 0.307, P = 0.009 for CD8+). On the contrary to membrane-bound TRAIL expression, serum level of sTRAIL was not correlated with that of TBIL and PT, though it was higher than that of the normal population and was positively correlated with serum HBeAg expression (r = 0.695, P = 0.001).
CONCLUSION: The expression level of TRAIL on the membrane of lymphocytes was upregulated and associated with the liver injury in CHB patients. These findings suggest that upregulation of TRAIL expression may be induced by virus antigen and inflammatory cytokine IFN-γ.