Supplementary Materials

This PDF file includes:

  • Fig. S1. Additional signaling analyses of CXCR3 ligands.
  • Fig. S2. Biased signaling is conserved at murine CXCR3.
  • Fig. S3. The inflammatory effects of the β-arrestin–biased agonist VUF10661 are absent in CXCR3 KO mice.
  • Fig. S4. Loss of β-arrestin2 attenuates chemotaxis to mCXCL10, and both VUF10661 and mCXCL10 induce chemotaxis of only CD44+ T cell populations.
  • Fig. S5. Biased ligands of CXCR3 differentially increased the numbers of CD4+CD44+ T cells and total T cells in DNFB-treated ears.
  • Fig. S6. Human T cell chemotaxis.
  • Fig. S7. Targeted phosphoprotein data in T cells, monocytes, and natural killer cells.
  • Fig. S8. Co-immunoprecipitation of pAkt-Thr308 with β-arrestin2.
  • Fig. S9. Differential phosphorylation of Akt, but not ERK1/2, in a T cell line stably expressing CXCR3 after stimulation with VUF10661 or VUF11418.
  • Fig. S10. Both PTX and a PI3K inhibitor eliminate effector T cell migration to VUF10661.
  • Fig. S11. Flow cytometry gating strategy.
  • Table S1. Pharmacological properties of the biased agonists of CXCR3.
  • Table S2. Flow cytometry antibodies.

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