Key resources used in the conduct of experiments is provided

Supplemental Figure 3. Compensatory mechanisms in CCR1 ablated tumor microenvironment elicits immune infiltration

Figure S1: IL-33+ stromal cells are abundant in human and mouse PDA.

Figure S3: Pancreatic fibroblasts secrete IL-33 in response to oxidative stress.

Oncogenic KRAS expression affects serum cytokine and chemokine concentration.

Fibroblast-specific STAT3 activation preferentially promotes lung, not liver, metastasis.

Figure S4: Loss of stromal IL-33 alters the ST2+ immune cell secretome, resulting in a shift in CAF differentiation.

Table S3. Single cell RNA sequencing datasets

Genetic and orthotopically injected pancreatic cancer models show KRAS-dependent premetastatic and metastatic niche formation.

Supplementary Figure 1 provides additional details of orthotopic tumors treated with TCDD including histology, gross pictures and dose escalation. Data on additional cell lines including in vitro growth kinetics is provided.

Histopathological analysis of human pancreatic cancer metastasis.

Supplementary Figure 5 shows additional single cell sequencing data from orthotopic PDAC tumors in mice treated with TCDD or untreated.

Table S1. Antibodies used for immunostaining, flow cytometry and CyTOF

Validation of lack of cancer cells in premetastatic samples.

Figure S7: Tumor cell-initiated autocrine signaling drives IL-33 upregulation in pancreatic fibroblasts.

Table S1. Single cell RNA sequencing datasets.

Supplementary Figure 2 shows RNA and protein expression of interferon gamma and IL22. An image of the standard ELISA curve is provided.

Figure S6: Expression of fibroblast IL-33 is extrinsically induced by epithelial KrasG12D and requires JAK1/2-STAT3 activation throughout tumorigenesis.

Figure S2: Stromal IL-33 promotes PDA growth.

Supplemental Figure 8. CD8 T cell activation upon CCR1 and ARG inhibition combined with anti–PD-L1 in PDA