Supplementary Materials
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 p38αNesCre mice.
- Fig. S4. The activity of p38α in CNS-resident cells is not required for peripheral TH17 and TH1 cell responses.
- Fig. S5. The activity of p38α in CNS-resident cells is dispensable for the initial infiltration of transferred TH17 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).