Supplementary Materials for:

Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis

Gonghua Huang, Yanyan Wang, Peter Vogel, Hongbo Chi*

*Corresponding author. E-mail: hongbo.chi{at}stjude.org

This PDF file includes:

• Fig. S1. Effects of p38α deficiency on immune signaling pathways in CNS inflammation.
• Fig. S2. Effects of late p38α deletion and IL-17 neutralization on EAE disease course.
• Fig. S3. p38α is specifically deleted in the CNS of p38α^NesCre mice.
• Fig. S4. The activity of p38α in CNS-resident cells is not required for peripheral T_H17 and T_H1 cell responses.
• Fig. S5. The activity of p38α in CNS-resident cells is dispensable for the initial infiltration of transferred T_H17 cells into the CNS, but contributes to proinflammatory gene expression.
• Fig. S6. Expression of IL-17R components and mechanisms of chemokine gene regulation in astrocytes.
• Fig. S7. Analysis of MKP-1 and JNK functions.

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Citation: G. Huang, Y. Wang, P. Vogel, H. Chi, Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis. Sci. Signal. 8, ra24 (2015).

© 2015 American Association for the Advancement of Science