Science Immunology

Supplementary Materials

The PDF file includes:

  • Material and Methods
  • Fig. S1. Test of knockout and knockdown efficiency in Il17rc KO mice and IL17RD knockdown human keratinocytes.
  • Fig. S2. IL-17RD functions as a receptor for IL-17A but not IL-17A/F in mouse keratinocytes.
  • Fig. S3. IL-17RC and IL-17RD are both required for the full development of IMQ-induced psoriasis-like skin inflammation.
  • Fig. S4. IL-17RD expression in keratinocytes is important for IMQ-induced psoriasis-like skin inflammation.
  • Fig. S5. Densitometry analysis of the phosphorylation of p38, IκB, Erk, and JNK in primary mouse keratinocytes.
  • Fig. S6. The expression of psoriasis-related genes in WT, Il17rd KO, Il17rc KO, and Il17rc and l17rd DKO keratinocytes stimulated with IL-17A.
  • Fig. S7. Secretion of CXCL1 and CCL20 from IL-17A–stimulated WT, Il17rd KO, Il17rc KO, and Il17rc and l17rd DKO keratinocytes.
  • Fig. S8. The expression of psoriasis-related genes in WT, Il17rd KO, and Il17rc KO keratinocytes stimulated with IL-17F or IL-17A/F.
  • Fig. S9. IL-17A–induced IL-23 expression was diminished by Il17rc KO, Il17rd KO, Act1 KO, and NF-κB or ERK inhibition.
  • Fig. S10. Reduced IL-23 level is associated with reduced IL-17 level in the skin of Il17rd KO mice.
  • Fig. S11. IL-17RD deficiency did not significantly reduce lipopolysaccharide and TNF-α signaling in mouse primary keratinocytes.
  • Fig. S12. Gating strategy for granulocytes, γδ T cells, and ILC3s.
  • Table S1. List of primer sequences used for RT-qPCR analysis.
  • Table S2. List of antibodies used in this study.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Complete list of differential regulated genes in Il17rd KO keratinocytes compared with WT upon IL-17A stimulation.
  • Data file S2 (Microsoft Excel format). Raw data.

Files in this Data Supplement: