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The spontaneous suppressor or helper T cell activity present in the peripheral blood was evaluated by measurring the capacity of T cells to help differentiation of B cells into plasma cells in response to pokeweed mitogen with increasing ratio of T: B in vitro culture. Peripheral T cells from patients with chronic active hepatitis (CAH) showed a significantly decreased suppressor effect (or increased helper effect) on allogeneic B cell differentiation into Ig-producing cells, when compared to healthy sugjects (p<0.01). After irradiation of T cells to eliminate suppressor cell influences and to evaluate genuine helper activity, helper activity of CAH was not different from that of healthy subjects, suggesting that spontaneous suppressor cell activity was significantly decreased in CAH.Con A-induced suppressor cell activity both on allogeneic B cell differentiation into Igproducing cells in presence of PWM and on allogeneic lymphocyte blast transformation responses to Con A was also significantly decreased in patients with CAH, when compared to healthy subjects (p<0.001). Similar Con A-induced suppressor cell defect was also observed in patients with chronic persistent hepatitis, but to lesser degree (p<0.05). There was no clear-cut difference in suppressor cell activity between patients with and without HBs antigen in the sera.Preincubation of lymphocytes from healthy persons with some CAH sera significantly decreased the Con A-induced suppressor T cell activity on lymphocyte blast transformation responses, suggesting that the factor (s) that modulate suppressor T cell activities was present in CAH sera.Autologous mixed lymphocyte reaction (AMLR) was significantly decreased in CAH patiens (p<0.005), when compared to healthy subjects. Reactivity of AMLR and Con-A induced suppressor activity when tested in the same patients, were correlated well (p=0.824, p<0.001, n=12). These results suggest that abnormal immunoregulatory functions may reflect more or less disease activity of chronic hepatitis and altered immune responses of CAH regardless of the presense of serum HBs antigen.
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