Sandro Vento was a recipient of an Anna Villa Rusconi Foundation Research Fellowship.
T lymphocyte sensitization to hbcag and T cell-mediated unresponsiveness to HBsAg in hepatitis B virus-related chronic liver disease
Article first published online: 6 DEC 2005
Copyright © 1985 American Association for the Study of Liver Diseases
Volume 5, Issue 2, pages 192–197, March/April 1985
How to Cite
Vento, S., Hegarty, J. E., Alberti, A., O'brien, C. J., Alexander, G. J. M., Eddleston, A. L. W. F. and Williams, R. (1985), T lymphocyte sensitization to hbcag and T cell-mediated unresponsiveness to HBsAg in hepatitis B virus-related chronic liver disease. Hepatology, 5: 192–197. doi: 10.1002/hep.1840050206
- Issue published online: 6 DEC 2005
- Article first published online: 6 DEC 2005
- Manuscript Accepted: 6 NOV 1984
- Manuscript Received: 15 MAR 1984
Using a newly developed indirect T lymphocyte migration inhibition test, cell-mediated immunity to HBsAg and HBcAg was directly and simultaneously examined in a total of 21 patients with HBsAg-positive chronic liver disease (CLD), and in seven subjects whose sera contained anti-HBs (2 previous acute hepatitis B; 4 hepatitis B vaccine recipients and 1 chronic active hepatitis). T cell sensitization to HBcAg was invariably detected in the HBsAg-positive CLD patients tested (12/12), whereas T cell sensitization to HBsAg was not present in any of the patients (0/21). In contrast, T cell sensitization to HBsAg was present in all anti-HBs-positive subjects.
These results support the hypothesis that the cellular immune response to HBcAg, rather than to HBsAg, is implicated in the pathogenesis of HBsAg-positive CLD. Moreover, the observation that the addition of T cells from patients with HBsAg-positive CLD to T cells from anti-HBs positive subjects in a ratio of 1 to 9 reversed their sensitization to HBsAg, suggests that a hyperactivity of HBsAg-specific suppressor T cell population may be responsible for persistent HBs antigenemia.