Besides invasion, network epidemiological models can also be used to understand patterns of geographical spread of endemic diseases [14] [15] [16] [17] . Many infectious diseases can only be maintained in a endemic state in cities with population size above a threshold, or under appropriate environmental conditions(climate, availability of a reservoir, vectors, etc). The variables and the magnitudes associated with endemicity threshold depends on the natural history of the disease [18] . Theses magnitudes may vary from place to place as it depends on the contact structure of the individuals. Predicting which cities are sources for the endemicity and understanding the path of recurrent traveling waves may help us to design optimal surveillance and control strategies. Autoimmune Cholangitis in the SJL/J Mouse is Antigen Non-specific Primary biliary cirrhosis (PBC) is an autoimmune disease characterized by intrahepatic bile duct destruction and the production of anti-mitochondrial antibodies (AMA). The absence of an animal model has been a striking impedance in defining the molecular basis of disease. Previous work has suggested that SJL/J mice immunize with the pyruvate dehydrogenase complex (PDC-E2), the major mitochondrial autoantigen of PBC, leads to the development of lymphoid cell infiltration in portal tracts and a model system coined autoimmune cholangitis. We hypothesized that this pathology would be augmented if immunization occurred in the presence of IFN-γ injections. Accordingly, SJL/J mice were immunized with PDC-E2 and, for purpose of control, α-casein. Subgroups of mice were also treated with exogenous IFN-γ. As expected, mice immunized with PDC-E2, with or without IFN-γ, developed high titer AMAs. In contrast, mice immunized with α-casein, develop antinuclear antibodies. More importantly, the livers from mice immunized with PDC-E2 and/or those immunized with α-casein all displayed lymphoid cell infiltration to the portal tracts, irrespective of bile duct size. Indeed, there was no significant difference between the experimental and the control groups by histologic analysis. Thus, autoimmune cholangitis in these mice is antigen non-specific. Primary biliary cirrhosis (PBC) is a chronic inflammatory, organ specific autoimmune disease of the liver characterized by high titer anti-mitochondrial antibodies (AMA) and intrahepatic bile duct destruction (Nakanuma and Ohta, 1979; Scheuer, 1994; Kaplan, 1996) . The etiology and pathogenesis of PBC are unknown. High titer AMA react with a series of highly conserved intramitochondrial proteins including the E2 subunit of the pyruvate dehydrogenase complex (PDC-E2), the major autoantigen of PBC. Whether liver injury is caused by AMA (Malmborg et al., 1998; Feehally and Allen, 1999) , PDC-E2 specific T cells (Van de Water et al., 1997; Shimoda et al., 1998; Inada et al., 2000) , NK cells (Tsuneyama et al., 1998; Iwata et al., 2000) or pathological alterations of the bile ducts themselves (Yasoshima et al., 1995; Kimura et al., 1996; Leon et al., 1997) are all being investigated. However, it is important to bear in mind that PBC is an autoimmune disease that most likely develops as a multi-hit disease, not just one insult. It has been theorized that PBC, in a genetically susceptible host, may be initiated by a molecular mimic (Coppel and Gershwin, 1995; Shimoda et al., 2000) or a xenobiotic (Uibo and Salupere, 1999; Long et al., 2001) . However, to this end, no definitive causative agent has, as yet, been identified.