Supplementary Materials

Supplementary Material for:

Insulin B chain 9–23 gene transfer to hepatocytes protects from type 1 diabetes by inducing Ag-specific FoxP3+ Tregs

Mahzad Akbarpour, Kevin S. Goudy, Alessio Cantore, Fabio Russo, Francesca Sanvito, Luigi Naldini, Andrea Annoni, Maria Grazia Roncarolo*

*Corresponding author. E-mail: mg1{at}stanford.edu

Published 27 May 2015, Sci. Transl. Med. 7, 289ra81 (2015)
DOI: 10.1126/scitranslmed.aaa3032

This PDF file includes:

  • Materials and Methods
  • Fig. S1. InsB9–23–specific CTL response is induced after ICLV.PGK and ICLV.PGK.142T treatment.
  • Fig. S2. InsB15–23–specific CD8+ T cells are functional in ICLV.ET.InsB9–23.142T–treated NOD mice.
  • Fig. S3. Genes related to immune regulation and FoxP3+ Tregs are up-regulated after ICLV treatment.
  • Fig. S4. TH1, TH2, and TH17 T cell subsets are not expanded by ICLV.ET.InsB9–23.142T treatment.
  • Fig. S5. Depletion of FoxP3+ Tregs from total splenocytes.
  • Fig. S6. CD8+ T cell response to IGRP is reduced in ICLV.ET.InsB9–23.142T–treated NOD mice.
  • Fig. S7. Transgene-specific CTL response is induced after IDLV treatment.
  • Fig. S8. Frequency of FoxP3+ Tregs is increased in pancreatic islet infiltration after IDLV treatment.
  • Fig. S9. IDLV treatment induces expression of FoxP3+ Treg–related genes.
  • Fig. S10. Efficacy of ICLV.ET.InsB9–23.142T treatment is reduced in hyperglycemic NOD mice, and it is abrogated in overt disease.
  • Fig. S11. Definition of the suboptimal and noneffective dose of anti-CD3 mAb.
  • Supporting material to Fig. 3A
  • Data tables
  • Reference (71)

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