Figure 1.

Wound healing and target killing are both effector mechanisms of CD8 T cells. (A) Combined proliferation and killing assay in the presence of influenza-specific CD8 T cells and varying amounts of pulsed peptides on MRC-5 and HaCaT cells seeded in a 30:70 ratio. Left, representative image with labels (0 versus 5 h; T cells only versus T cells + 100 ng/ml peptide). Right, representative quantification of Cas3/7 activity (green) and HaCaT proliferation (red) with titrated amounts of influenza peptide, with statistical verification across experiments using normalized area under the curve (AUC, n = 3, one-way ANOVA, symbols indicate individual experiments). Scale bars = 400 µm; enhanced for improved visibility. (B) SN from A tested in a wound healing assay with HaCaT cells; representative example with additional experiments in Fig. S1 (n = 3). Scale bars = 400 µm; enhanced for improved visibility. Reuse of the B panel in schematic of Fig. S1 A. (C) Measurement of intracellular TNF and IFN-γ in influenza-specific T cells used in the combined proliferation and killing assay, representative stainings (n = 12, one-way ANOVA), gating in Fig. S1. (D) Fold induction of AREG and TGFα in SNs from (A) (n = 3–4, one-way ANOVA, symbols indicate individual experiments) Individual experiments in Fig. S1. (E and F) Effect of using Cetuximab or anti-IFN-γ on wound healing capacity of SNs from (A) using background-corrected AUCs (n = 4, one-way ANOVA of AUC, symbols indicate individual experiments). Scale bars = 400 µm; enhanced for improved visibility. All data derived from three or more independent experiments.