Figure 8.

Pathogenesis of immune-mediated apoptotic liver injury. The liver has big population of Kupffer cells, dendritic cells, NK cells, and NKT cells. An innate immune response is initiated when antigens are presented by antigen-presenting cells (APCs) which then activate, directly and/or indirectly, NKT cells and other innate immune cells. The apoptosis of biliary epithelial cells (BECs) is a potential source of ‘neo-antigens' that may be responsible for facilitating molecular mimicry or autoimmunity. NKT cells upregulate FasL on their surface which binds to the Fas receptor expressed on target hepatocytes, leading to apoptosis. Activation of NKT cells can also indirectly induce hepatocyte apoptosis through the release of cytokines, including IFNγ and TNFα. Th2 responses are also induced due to the presence of IL-4, which then promote maturation of B cells into plasma cells for the production of autoantibodies. Furthermore, IL-17 family has been linked to many immune/autoimmune-related diseases