Supplementary Materials

Supplementary Material for:

Melanocortin-1 receptor activation is neuroprotective in mouse models of neuroinflammatory disease

Nadine Mykicki, Alexander M. Herrmann, Nicholas Schwab, René Deenen, Tim Sparwasser, Andreas Limmer, Lydia Wachsmuth, Luisa Klotz, Karl Köhrer, Cornelius Faber, Heinz Wiendl, Thomas A. Luger, Sven G. Meuth, Karin Loser*

*Corresponding author. Email: loserk{at}uni-muenster.de

Published 26 October 2016, Sci. Transl. Med. 8, 362ra146 (2016)
DOI: 10.1126/scitranslmed.aaf8732

This PDF file includes:

  • Fig. S1. α-MSH down-regulates the expression of markers associated with axonal damage.
  • Fig. S2. α-MSH inhibits EAE development by reducing the activity, antigen-specific proliferation, and cytokine secretion in pathogenic TH1 and TH17 cells.
  • Fig. S3. α-MSH expands immunosuppressive Treg in the regional lymph nodes from MOG-immunized mice.
  • Fig. S4. Signaling through a functional Mc1r is essential for the α-MSH–mediated prevention of EAE.
  • Fig. S5. NDP-MSH generates tolerogenic DCs with a reduced capacity to expand CD4+ effector T cells.
  • Fig. S6. MSH efficiently inhibits the progression of ongoing EAE in wild-type mice.
  • Fig. S7. Depletion of DCs or Treg in DT-treated CD11c.DOG or DEREG mice, respectively.
  • Fig. S8. Functional protein association networks and pathway classification of gene expression data from the CNS of MOG-immunized mice treated with PBS or NDP-MSH at disease maximum.
  • Fig. S9. Under inflammatory or excitotoxic conditions, Mc1r ligation up-regulates Nr4a1 and allows action potential generation.
  • Fig. S10. Disease progression and numbers of TH17, TH1, as well as Treg cells in the CNS of bone marrow chimeric mice.
  • Fig. S11. Nr4a1 expression in nonhematopoietic cells of the brain.
  • Table S1. Sequences of primers used to amplify mouse and human genes.
  • Data values

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