Cell - 8 September 2016

Figure S3. Selective Blockade of Chemokine Signaling MitigatesgdT Cell Expansion and Activation in PDA and Deletion or Depletion ofgdT
Cells or Interruption of Their Recruitment Is Protective against PDA, Related toFigure 3
(A–E) WT, CCR2–/–, CCL2–/–, CCR5–/–, and CCR6–/–mice were orthotopically implanted with KPC-derived PDA cells (n = 5/group). Animals were sacrificed at
3 weeks. (A) The fraction of tumor-infiltratinggdT cells determined by flow cytometry.gdT cell expression of (B) TNF-a, (C) IL-13, (D) IL-17, and (E) IFN-gwas
determined for each cohort (n = 5 /group).
(F) WT mice were treated with UC3-10A6 and splenocytes from these mice were analyzed for expression of Vg4 and Vg1.
(G) WT and Tcrd–/–pancreata were orthotopically implanted with KPC-derived PDA cells. Tumors were harvested and weighed at 3 weeks after implantation.
Representative gross images of PDA and quantitative data of tumor weights are shown (n = 10/group).
(H) Pancreata from control WT mice, WT mice treated with a neutralizinga-gdT cell mAb, and Tcrd–/–mice were orthotopically implanted with KPC-derived PDA
cells. Kaplan-Meier survival analysis was performed (n = 10/group; WT versus Tcrd–/–: p = 0.02; WT versus UC3-10A6: p = 0.009; Tcrd–/–versus UC3-10A6:
p = ns).
(I) WT, CCR5–/–, CCR6–/–, CCR2–/–, and CCL2–/–mice were orthotopically implanted with KPC-derived PDA cells. Animals were sacrificed at 3 weeks and tumor
weights were recorded. Data from 2 separate experiments are shown (n = 5/group for each experiment; scale bar = 2cm; *p < 0.05, p < 0.01, **p < 0.0001).