Interferon-β Therapy Against EAE Is Effective Only When Development of the Disease Depends on the NLRP3 Inflammasome

Makoto Inoue, Kristi L. Williams, Timothy Oliver, Peter Vandenabeele, Jayant V. Rajan, Edward A. Miao, Mari L. Shinohara*

*To whom correspondence should be addressed. E-mail: mari.shinohara{at}duke.edu

This PDF file includes:

• Fig. S1. IFNAR signaling suppresses activation of the NLRP3 inflammasome.
• Fig. S2. IFNAR signaling does not inhibit pro–IL-1β production.
• Fig. S3. IFNAR signaling inhibits the formation of caspase-1 foci.
• Fig. S4. IFNAR signaling does not affect expression of Nlrp3, Asc, Casp-1, and Txnip or the abundance of P2X7R and CD39, but does induce ROS generation.
• Fig. S5. ROS generated by mitochondria, but not by NADPH oxidase, is suppressed by type I IFN.
• Fig. S6. Inhibition of Rac1 inhibits the production of IL-1β and ROS, but does not affect the expression of Tnf, Il6, or Il1b.
• Fig. S7. Involvement of SOCS1 in IFNAR signaling.
• Fig. S8. Events upstream of the NLRP3 inflammasome are intact in NLRP3 inflammasome–deficient macrophages.
• Fig. S9. Serum IL-18 concentrations 9 days after immunization.
• Fig. S10. Evaluation of rIFN-β efficacy in cell culture.
• Fig. S11. IFNAR signaling suppresses NLRP3 inflammasome activity in vivo.
• Fig. S12. NLRP3 inflammasome–dependent and –independent EAE.
• Fig. S13. Inflammasome activity in mice with passive EAE.
• Table S1. Sequences of primers used for qPCR analysis.
  

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© 2012 American Association for the Advancement of Science