SUMMARYExperimental autoimmune hepatitis (EAH) is an animal model for autoimmune hepatitis. The disease is T cell-mediated and runs a subacute course, with maximal disease activily around week four after disease induction and a slow ensuing recovery. The aim ofthe present sludy was lo investigate the immunoregulatory mechanisms that may account for recovery in EAH. It was found thai T cell reactivity to liver antigens preceded hislological disease, but at the peak of disease activily this Tcell response was already suppressed. Active and antigen-specific suppression could be demonstraied, as irradiated splenocytes frotn animals at lhe beginning of recovery from EAH were able to suppress in vitro the T cell response to liver antigens by 42%. The response to an irrelevant antigen was suppressed by 16%. showing additional antigen non-specific suppression in vitro. The response lo an inivro immunization with an unrelated mierobial antigen (telanus toxoid)at the peak of disease was markedly reduced (by 90%). These data demonstrate in vitro and in vivo immunosuppression associated with the overcoming of and recovery from EAH. They stress the importance of immunoregulatory cycles in the control of autoimmune hepatitis.

ABSTRACT— Three substances (pronase E, sodium dodecylsulfate (SDS) and guanidine hydrochloride) with different chemical actions partially convert HBcAg to HBeAg. This process retains the integrity of the HBcAg particle, which was not different between HBcAg subpopulations, and does not generate HBcAg or HBeAg sub‐units. DNA polymerase activity was destroyed by SDS and guanidine hydrochloride, but not by pronase E. Serum HBeAg could not be converted into HBcAg, suggesting that this might be an irreversible process. The data are consistent with the assumption that HBcAg and HBeAg are coded for by the same gene (C gene of the HBV‐DNA).

It has recently been irrlicated that 9ffb of patie'lts wi1h liver disease seo::ndary to Cystic Fjj)rosis (CF)-evidence of carm:n bile dJct sterosis rn hepatooiliary scarnirg (Gaskin et Al:N.El1g.J.Med,316:34:J,l!llB).We performed IDA sca1 pre am 10