Inhibition of lymphocyte cytotoxicity in chronic active hepatitis.

Inhibitory factors were investigated, using 51Cr-labelled Chang cells as targets, based on the inhibition of lymphocyte-mediated cytotoxicity (LMC) in patients with chronic active hepatitis (CAH). A significant reduction of LMC was noted (P less than 0.001) when autologous sera of patients with CAH was added. The addition of HBsAg-positive and -negative homologous sera from CAH, which were as capable of inhibiting LMC as autologous sera, decreased LMC significantly (P less than 0.001). The LMC fell significantly (P less than 0.001) in the presence of sera of patients with rheumatoid arthritis. A significantly higher inhibition (P less than 0.001) by rheumatoid factor (RF) positive autologous sera of patients with CAH was observed when compared to that of RF-negative sera. Such autologous sera inhibiting LMC contained increased IgG levels (P less than 0.01) when compared to those that failed to inhibit LMC. A significant reduction of LMC was also induced with the addition of anti-HBs (P less than 0.05), HBsAg--anti-HBs (P less than 0.001) and IgG--anti-IgG (P less than 0.01) complexes, or aggregated IgG (P less than 0.001). The LMC was reduced significantly (P less than 0.001) after adding a purified liver-specific membrane lipoprotein (LSP) from human livers. There was some evidence for the inhibition of LMC being effected by these additives as a result of their acting on an effector cell level. These findings suggest that humoral factors including immune complexes, aggregated IgG and LSP play an important role for lymphocyte cytotoxicity in the pathogenesis of CAH.