Supplementary Materials

Supplementary Material for:

Epidermal EGFR Controls Cutaneous Host Defense and Prevents Inflammation

Beate M. Lichtenberger, Peter A. Gerber, Martin Holcmann, Bettina A. Buhren, Nicole Amberg, Viktoria Smolle, Holger Schrumpf, Edwin Boelke, Parinaz Ansari, Colin Mackenzie, Andreas Wollenberg, Andreas Kislat, Jens W. Fischer, Katharina Röck, Jürgen Harder, Jens M. Schröder, Bernhard Homey,* Maria Sibilia*

*Corresponding author. E-mail: maria.sibilia@meduniwien.ac.at (M.S.); bernhard.homey@uniduesseldorf. de (B.H.)

Published 21 August 2013, Sci. Transl. Med. 5, 199ra111 (2013)
DOI: 10.1126/scitranslmed.3005886

This PDF file includes:

  • Fig. S1. EGFRI effectively blocks EGFR signaling in the skin.
  • Fig. S2. EGFRI differentially regulates the expression of various chemokines.
  • Fig. S3. EGFR is effectively deleted in epidermal cells.
  • Fig. S4. Deletion of EGFR in adult mice results in a benign skin phenotype.
  • Fig. S5. Mice treated with erlotinib do not display the skin inflammation found in EGFRΔep mice.
  • Fig. S6. Lack of epidermal EGFR results in skin inflammation.
  • Fig. S7. EGFRΔep mice display strong skin inflammation.
  • Fig. S8. EGFRΔep mice display an epidermal differentiation defect.
  • Fig. S9. EGFRΔep mice are not rescued in a Rag2-, CCL2-, MyD88-, or LCdeficient background.
  • Table S1. Patient characteristics.

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Other Supplementary Material for this manuscript includes the following:

  • Table S2. Raw data of experiments with fewer than 20 biological replicates (Excel file).

[Table S2]