Fig. 3

ConA-induced hepatitis is controlled by Par2 activation in the immune system. A, C, and D FACS analysis of CD45.2 mice (WT and Par2KO) that were used as BM donors to reconstitute WT CD45.1 mice, indicate that T-lymphocyte distribution after BM replacement was comparable in both setups, as both CD4 and CD8 T cells comprised an average of 88% of the donor T cells (C), n=14. B, C, and D. The reciprocal experiment: FACS analysis of WT CD45.1 that were used as BM donor to CD45.2 (WT and Par2KO) recipient mice. T cell distribution after BM replacement remained the same in both setups. The donor cells comprise ~81% of the T cells, n=22. Red circles indicate mice that were excluded from the experiment due to unsuccessful BM replacement (n=3). E, H A control experiment WT BM-reconstituted WT mice (CD45.1 into CD45.2) displays both mononuclear cell infiltration and hepatocellular damage. Note that hepatocellular damage is apparent on day 1 (E). F, I Par2KO BM-reconstituted WT mice show the relatively diminished levels of infiltrates. Note that hepatocellular damage is still apparent. G, J WT BM-reconstituted Par2KO mice. Infiltrates and tissue damage are apparent, indicating that mononuclear infiltrations are mediated via Par2 on immune cells and not via Par2 signaling in the hepatic tissue. Scale bar =75μm. K Quantification of the hepatocellular damage (the percentage area of necrotic lesions) presented in E–J (n=18, 3 for each group). Black—statistical significance within the same group. Red—statistical significance in comparison to control at day 1. Blue—statistical significance between the two reciprocal BM replacements. Statistical significance was measured using T test. *Indicates p<0.05, **p<0.01, ***p<0.005, error bars = SEM