Supplementary Materials

This PDF file includes:

  • Fig. S1. Analysis of pSmad2/3 abundance in CD4+ T cells treated with TGF-β, ivermectin, and SB-431542.
  • Fig. S2. Representative profiles of OCR and ECAR measurements of quiescent and activated T cells as assessed with an extracellular flux analyzer.
  • Fig. S3. Inhibition of CD4+ T cell mitochondrial respiration by TGF-β requires Smad phosphorylation, but not nuclear localization.
  • Fig. S4. Knockdown efficiency of Smad2-specific siRNA in human primary CD4+ T cells and Jurkat cells.
  • Fig. S5. CD4+ T cells differentiated with TGF-β to induce FoxP3+ Treg cells demonstrate increased mitochondrial SRC.
  • Fig. S6. TGF-β decreases mTORC1 activity in CD4+ T cells, and the TGF-β–mediated decreases in CD4+ T cell mitochondrial respiration are partly mTORC1 dependent.
  • Fig. S7. Treatment of effector memory CD4+ T cells with TGF-β decreases oxygen consumption in response to provision of specific substrates for complexes I, II, III, and IV.
  • Fig. S8. Effector memory CD4+ T cells are more susceptible to TGF-β–mediated IFN-γ suppression than are naïve or central memory cells, consistent with increased TGF-βRII abundance and signaling.
  • Fig. S9. Inhibition of ETC complexes I, II, III, and IV suppresses IFN-γ production by effector memory CD4+ T cells.
  • Fig. S10. Effects of SB-431542 and ivermectin on CD4+ T cell IFN-γ production as measured by intracellular staining or ELISA.
  • Table S1. Clinical details for tumor effusion samples.
  • Table S2. Primer sequences used for the quantification of mRNA by PCR.

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