Impaired concanavalin A-inducible suppressor T-cell activity in active alcoholic liver disease.

To examine the possible contribution of cellular immunoregulatory mechanisms to the pathogenesis and progression of alcoholic liver diseases, suppressor T-cell function was evaluated in patients with severe active or inactive alcoholic liver disease and compared with normal control subjects. Suppressor T-cell activity after in vitro induction by concanavalin A or other T cell-mediated immune reactions was then assessed. T-cell interactions studied included the proliferative responses of both autologous or allogeneic responding peripheral blood mononuclear cells to T-cell mitogens and to allogeneic cells. No significant differences were found in the ability to induce suppressor T cells between controls and patients with inactive alcoholic liver disease (p < 0.05). In contrast, T cells from patients with severe active alcoholic liver disease failed to develop suppressor cell activity (p < 0.001) after concanavalin A stimulation; restoration of suppressor cell function was found after these patients improved clinically. Adherent cells (monocyte-macrophages) from patients with active alcoholic liver diseases exhibited normal support of concanavalin A-induced blastogenesis and suppressor T-cell generation. This immunoregulatory cell abnormality could be important in the pathogenesis and/or progression of active alcoholic liver disease.