In order to avoid graft rejection, liver transplantation requires chronic immunosuppression that can cause complex immune system alterations, most of them are until now quite incompletely understood. Among these, chronic rejection and the increased susceptibility to infections remain probably the major concerns of organ transplantation.
Recently, a peculiar form of a so called “autoimmune” disease was described after liver allograft transplantation, characterized by a clinical picture of chronic hepatitis and by the presence of circulating auto-antibodies. This type of graft dysfunction has been defined as de novo autoimmune hepatitis.
This funny pathology arises in patients transplanted for diseases other than autoimmune hepatitis and without signs of systemic autoimmune disease, usually as a long-term complication.  The clinical and pathological picture is probably very different and more complicated than that of autoimmune hepatitis observed in non-transplanted patients. 
De novo autoimmune hepatitis seems to be more frequent in the pediatric population (about 4% of liver transplanted children) than in the adult one. 
Clinical signs of chronic hepatitis can be seen at a variable degree; blood auto-antibodies are the rule, high blood transaminase levels and high Immunoglobulin (IgG) titers are often associated.
Histology shows lymphocytic infiltrate with interface hepatitis $ and lobular hepatitis $, sometimes associated with confluent necrosis. 
Severity range of clinical and morphological lesions is extremely variable.
The treatment of this complication was successful, as reported by several liver transplant centers, using steroids and Azathioprine until disappearance of the clinical and histologic signs of disease.
Our experience was focused on 5 pediatric patients, mostly receiving liver transplantation for biliary atresia, who showed evidence of de-novo autoimmune disease; the diagnosis was very complicated in the first two cases because of the presence of a clinical picture peculiar for Post Transplant Lymphoproliferative disease (PTLD) and the overlapping features of rejection episodes. As a matter of fact, the subsequent cases were more clearly identified and an adequate therapy promptly administered. The results were satisfactory and in all cases the remission of disease was obtained. 
This clinical experience has also increased our attention on the risk of all transplanted patients to be exposed to de-novo hepatitis, so that all our liver transplant recipients are now being investigated for the presence of clinical, humoral and histologic autoimmunity markers.
Further studies are now going on to understand more clearly the pathogenesis of this disease and its relationship with infection and chronic rejection. Also remain to be investigated the long-term outcome of patients and grafts, and the possibility of more appropriate medical treatment of the disease.