As shown in Fig. 1B, IFN-γ and IL-4 were produced dominantly by hepatic iNKT (CD3+CD1d tetramer+) cells. Similarly, to analyze the antigen-presenting capacity of DCs, we evaluated surface marker expression 24 hours after α-GalCer injection compared to controls. Significantly increased expression levels of MHC class I (H-2Kb),

MHC class II (I-Ab), CD1d, CD80, CD86, and CD40 on DCs (CD11c+NK1.1− cells) in liver and spleen of mice administered with α-GalCer was noted compared to that of mice administered with PBS (Fig. 1C), suggesting that α-GalCer intravenously stimulated selleck kinase inhibitor the full maturation of DCs in liver and spleen. Four weeks postimmunization, serum autoantibodies IgM and IgG to PDC-E2 were significantly increased in α-GC/CFA/2-OA mice as compared to that of PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 2A). Importantly, there was a significant increase in liver inflammation, portal inflammation, and bile duct damage in the α-GC/CFA/2-OA group compared to PBS/CFA/2-OA mice (Fig. 2B,C; Table 1). Further, ductular proliferation was observed in four out of five α-GC/CFA/2-OA mice but not in any (0/5) of the PBS/CFA/2-OA mice (Table 1). Furthermore, mild fibrous septa extension PD0325901 concentration (score = 2) was observed in three out of five α-GC/CFA/2-OA mice (Fig. 2C; Table 1). In addition,

there was significantly increased MHC class I, II, and costimulatory molecules CD86 and CD40 expression on the DCs of α-GC/CFA/2-OA mice compared to PBS/CFA/2-OA mice (Fig. 2D). There was a significant increase the in liver total mononuclear cells in α-GC/CFA/2-OA mice compared

to that of PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 3A). In addition, significantly increased numbers of conventional T (CD3+ NK1.1−) cells and B cells were noted in α-GC/CFA/2-OA mice (Fig. 3B). Importantly, significantly increased absolute numbers of CD8+ T cells were noted in α-GC/CFA/2-OA mice compared to that of PBS/CFA/2-OA mice (Fig. 3C). Serum autoantibodies IgM and IgG to PDC-E2 were significantly increased in α-GC/CFA/2-OA mice as compared to PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 4A). Examination of H&E-stained liver section revealed portal inflammation, bile duct damage, granulomas, proliferating bile ductules, and fibrous septa extension in the α-GC/CFA/2-OA group (Fig. 4B). In the α-GC/CFA/2-OA group, minimal to moderate (score = 1-3) liver inflammation, portal inflammation, and bile duct damage were observed (Fig. 4C; Table 1). Granulomas were found in 12/13 α-GC/CFA/2-OA mice (Fig. 4C; Table 1). In addition, fibrous septa extension was observed in all (13/13) α-GC/CFA/2-OA mice examined (Table 1). It is also important to note, as shown in Fig. 4D and Table 1, that 10/13 α-GC/CFA/2-OA mice demonstrated liver fibrosis as highlighted by silver staining and Azan staining.