Last update:
05-Aug-2017

It is well-established that the liver is an organ biased to tolerance. The liver tolerance effect is demonstrated mainly by persistent infection by pathogens such as hepatitis B and C viruses (HBV and HCV), as well as Plasmodium falciparum, and establishment of metastatic tumors in the liver. Immune tolerance in the liver can, however, be broken, resulting in robust hepatic immunity against pathogens and sometimes immune-mediated liver damage. Immune tolerance to self-antigens in the liver can also break down, leading to autoimmune liver disease. The tolerogenic properties of the liver are also demonstrated by the spontaneous acceptance of liver transplants in many species without the requirement of immunosuppression. Recently an interaction demonstrated between non-hematopoietic non-parenchymal liver cells and T-effector cells gave birth to the concept of a negative feedback mechanism described under the term mesenchyme-mediated immune control (MMIC). According to this theory, liver mesenchymal cells interact with interferongamma generated by alloreactive T-effector cells, resulting in up-regulated B7-H1 expression. The interaction between B7-H1 and its ligand leads to the apoptotic death of T-effector cells. The aim of this experimental study was to investigate whether inadequate expression of interferon-gamma and B7-H1 pathways may eventually lead to inadequate interaction between T-effector cells and mesenchymal cells that will in turn result in deficient MMIC.

Key words: Autoimmune hepatitis, Immunity, Liver tolerance, Rejection.