Fig. 3: Knocking out GITRL in liver progenitor cells reduced liver inflammation, fibrosis and ductular reaction. | Cell Death & Disease

Fig. 3: Knocking out GITRL in liver progenitor cells reduced liver inflammation, fibrosis and ductular reaction.

From: GITRL impairs hepatocyte repopulation by liver progenitor cells to aggravate inflammation and fibrosis by GITR+CD8+ T lymphocytes in CDE Mice

Fig. 3: Knocking out GITRL in liver progenitor cells reduced liver inflammation, fibrosis and ductular reaction.

A Experimental design strategy of Sox9Cre-ERTnfsf18flox/flox mice given a single dose of tamoxifen to inactivate GITRL followed by CDE injury after 2 weeks of tamoxifen washout. B Tissue mRNA transcript levels of Collagen I, Collagen III, and GITRL at 9 weeks in the CDE-treated Sox9Cre-ERTnfsf18+/+ mice or Sox9Cre-ERTnfsf18flox/flox mice and their control mice. C Representative flow cytometry images and statistical quantifications of the proportion of GITRL+Sox9+ or Sox9+EpCAM+ liver progenitor cells among the CD45 ̶ liver nonparenchymal cells at 9 weeks in the CDE-treated Sox9Cre-ERTnfsf18+/+ mice or Sox9Cre-ERTnfsf18flox/flox mice and their control mice. D Liver sections were examined for HE (upper panel), Sirius red (middle panel), and CK19/DAPI (lower panel). E Serum ALT and AST levels of each group at 9 weeks after CDE exposure.

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