Supplementary Materials

Supplementary Materials for:

p38α signaling in Langerhans cells promotes the development of IL-17–producing T cells and psoriasiform skin inflammation

Tingting Zheng, Weiheng Zhao, Hongjin Li, Shuxiu Xiao, Ran Hu, Miaomiao Han, Heng Liu, Yeqiang Liu, Kinya Otsu, Xinguang Liu, Gonghua Huang*

*Corresponding author. Email: gonghua.huang{at}shsmu.edu.cn

This PDF file includes:

  • Fig. S1. p38α deletion in mouse skin tissue and DCs.
  • Fig. S2. Normal DC development and activation status in the epidermis and dermis of p38αΔDC mice.
  • Fig. S3. Cell infiltration analysis in the skin and spleen of WT and p38αΔDC mice upon IMQ treatment.
  • Fig. S4. Gene expression in KCs and cytokine production in skin tissue of WT and p38αΔDC mice upon IMQ treatment.
  • Fig. S5. Decreased IL-17 production from γδ and CD4+ T cells in the skin and DLNs of p38αΔDC mice.
  • Fig. S6. The proliferation and apoptosis of T cells in IMQ-treated WT and p38αΔDC mice.
  • Fig. S7. p38α activity in LCs is important for psoriasiform skin inflammation.
  • Fig. S8. LC p38α-mediated TH17 cell differentiation and IL-23, IL-1β, and IL-6 expression.
  • Fig. S9. The effect of p38α signaling in DCs on skin inflammation is IL-1β–independent.
  • Fig. S10. p38α in dDCs affects IL-17 production from CD4+ T cells but not γδ T cells.
  • Fig. S11. p38α activity in T cells does not contribute to the IMQ-induced psoriasiform skin inflammation.
  • Fig. S12. Decreased IL-17 production from γδ and CD4+ T cells in the DLNs upon SB203580 treatment.
  • Fig. S13. Acute deletion of p38α reduces the severity of an ongoing psoriasiform skin inflammation.

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