Antigen specific suppressor T cells from chronic hepatitis B virus (HBV) carriers inhibit the responsiveness to HBsAg of allogeneic high-responder lymphocytes.

Immunoregulatory mechanisms in chronic HBsAg carriers have been investigated through the study of in vitro proliferative responses to HBsAg by allogeneic coculture experiments between T lymphocytes from HBsAg + chronic active hepatitis (CAH) patients (HBsAg no responder) and PBMC from subjects boosted with anti-hepatitis B vaccine (high responder). When high-responder PBMC have been challenged with the hepatitis B surface antigen (HBsAg) in the presence of HBsAg no-responder T lymphocytes, HBsAg no-responder T lymphocytes caused an antigen specific, dose-dependent, suppression of the responsiveness of high-responder PBMC. On the other hand, T cells from patients with autoimmune CAH did not exert any suppressor effect in our system. The suppressor T lymphocytes were mitomycin C resistant and were positive for OKT8, but were negative for OKT4. When T8 + cells were depleted from HBsAg no-responder PBMC, the in vitro immunoproliferative response to HBsAg in chronically HBV infected patients was markedly improved. Out data clearly demonstrate the existence of T8 + suppressor T lymphocytes that can control low responsiveness to HBsAg in chronic HBV patients.