Science Immunology

Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Top 15 regulated pathways associated with fibrosis in NASH and HCV.
  • Fig. S2. Identification of IL-17–producing, TH17, and Treg cells by flow cytometry in fresh liver biopsies and by IF in FFPE liver biopsies.
  • Fig. S3. Image processing and definition of region of interest.
  • Fig S4. Neutrophils represent the majority of IL-17 and IL-22 producing cells in the liver of humans and mice during chronic hepatitis.
  • Fig. S5. IL-22 enhances TGF-β responses in primary human HSCs independent of TGF-β receptor expression.
  • Fig. S6. IL-22 induces a proliferative and antiapoptotic phenotype in primary human stellate cells.
  • Fig. S7. IL-22 signaling is not required for control of hepatic inflammation during chronic liver injury.
  • Fig. S8. IL-22 enhances liver fibrosis during chronic TAA-mediated hepatic injury.
  • Fig. S9. Chronic liver injury induces activation of regulatory T cells in both WT and IL-22RA1 KO.
  • Fig. S10. Phenotypic characterization of intrahepatic IL-17– and IL-22–producing cells during chronic liver injury.
  • Fig. S11. Histology of the heart, lung, and kidney after therapeutic intervention with antagonist of AHR and RORγt.
  • Fig. S12. Inhibition of IL-22–producing cells with AHR or RORγt antagonists reduces liver fibrosis in TAA-induced injury.
  • Fig. S13. Treatment with RORγt antagonist reduces the number of IL-17–producing neutrophils and correlates with fibrosis reduction.
  • Fig. S14. Full Western blots from main figures.
  • Table S1. Patients’ characteristics and demographics.

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Other Supplementary Material for this manuscript includes the following:

  • Table S2 (Excel file). Raw data and statistics for all figures.

Files in this Data Supplement: