Fig. 4. NASH-driven fibrosis is partly TGF-β–dependent.

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Fig. 4. NASH-driven fibrosis is partly TGF-β–dependent. NASH-driven fibrosis is partly TGF-β–dependent. (A) WT mice were maintained for 40 weeks on a normal diet (filled symbols) or HFD (open symbols) and received 4 weeks of semiweekly control (Cont.) immunoglobulin (Ig) (squares) or anti–TGF-β (triangles) (250 μg each). Mice were assessed for obesity by MRI body composition measurement (n = 5 to 9) and hepatomegaly by liver weight and liver index scores (n = 5 to 12). (B) Hepatic triglycerides were measured, and fibrotic fraction was calculated by measuring picrosirius red–stained liver sections for characteristic NASH-associated fibrosis (n = 4 to 12). (C) Expression of four fibrosis-associated genes was measured (n = 5 to 12). Phorbol 12-myristate 13-acetate (PMA)/ionomycin–restimulated hepatic CD4 T cell production of IFN-γ, IL-4 (D), and IL-13 (left) (E) was assessed by intracellular cytokine staining (n = 5 to 10). (E) Expression of the type 2 inflammation marker chi3l3 was quantified from whole liver tissue (n = 4 to 11) (right). Freq., frequency. All data points represent a single mouse, and representative or pooled data from two or more independent experiments are shown (two-tailed t tests, n = 2 to 10; *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.0001). Kevin M. Hart et al., Sci Transl Med 2017;9:eaal3694 Published by AAAS