Supplementary Materials

The PDF file includes:

  • Fig. S1. SMs do not prevent activation and proliferation of TH17 cells.
  • Fig. S2. SMs promote NIK-dependent production of TNF in TH17 cells.
  • Fig. S3. SMs do not alter RORγt, IRF4, or BATF protein amounts in TH17 cells.
  • Fig. S4. Single cIAP deficiency cannot recapitulate SM-induced inhibition of TH17 cell differentiation.
  • Fig. S5. Proteomic changes in TH17 cells compared to undifferentiated CD4+ T cells.
  • Fig. S6. SMs induce global transcriptional and proteomic changes in TH17 cells.
  • Fig. S7. Reduced abundance of metabolic proteins in TH17 compared to undifferentiated CD4+ T cells.
  • Fig. S8. SM increases the abundance of noncanonical NF-κB and cell adhesion proteins in TH17 cells.
  • Fig. S9. RelB induces the expression of Nfkb2 and reduces the expression of Il17a independently of p52.
  • Fig. S10. SM treatment hinders RORγt binding to Il17a regulatory regions and increases the expression of immune checkpoint receptors in TH17 cells.
  • Fig. S11. SM depletion of cIAP1 but not xIAP activates the noncanonical NF-κB and does not alter the nuclear translocation of TH17-associated TFs.
  • Legends for data files S1 to S4

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Differentially expressed genes in DMSO- versus SM-treated TH17 cells.
  • Data file S2 (Microsoft Excel format). Differentially expressed proteins in DMSO- versus SM-treated TH17 cells.
  • Data file S3 (Microsoft Excel format). Proteins and pathways differentially regulated in TH17 compared to undifferentiated cells.
  • Data file S4 (Microsoft Excel format). Proteins and pathways differentially regulated in DMSO- and SM-treated TH17 cells.