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. 2021 Jan 29;12(1):141–157. doi: 10.1016/j.jcmgh.2021.01.016

Figure 8.

Figure 8

Loss of hepatocyte CD73 results in spontaneous liver inflammation. (A) Representative H&E images of inflammatory lesions in livers from 22-week-old CD73-LKO mice. Boxed areas in the top panels are magnified in the bottom panels. (B) Quantification of blinded histologic analysis of portal and lobular inflammation (scores were averaged for animals with portal + lobular inflammation). Scoring: 0, none; 2, minimal; 4, mild; 6, moderate; 8, severe. (C) Total liver messenger RNA analysis of proinflammatory markers interleukin 1β and tumor necrosis factor α in male (blue) and female (red) mice aged 21–42 weeks. (D) Representative images of immunohistochemical-stained paraffin-embedded liver tissues for neutrophil marker Ly6G (brown). Harris hematoxylin-stained nuclei (blue). Inset: magnified view of the boxed area showing signal distribution. Scale bar: 200 μm. (E) Quantification of Ly6G+ cells per view field in panel D. (F) Gene expression analysis of ectonucleotidase CD39 (Entpd1) and adenosine receptors A1R, 2AR, 2BR, and 3R (Adora1, 2a, 2b, 3) using total liver messenger RNA in male and female WT and LKO mice. n = 13 WT male, n = 12 LKO male, n = 14 WT female, n = 18 LKO female. ∗P < .05, ∗∗P < .01, ∗∗∗∗P < .0001, unpaired t test. Error bars represent SD.