Supplementary Table S1 and Figures S1 - S28 from IFNγ and CCL2 Cooperate to Redirect Tumor-Infiltrating Monocytes to Degrade Fibrosis and Enhance Chemotherapy Efficacy in Pancreatic Carcinoma
Authors: Long Kristen B. , Gladney Whitney L. , Tooker Graham M. , Graham Kathleen , Fraietta Joseph A. , Beatty Gregory L. 
Published: April 2023

<p>Supplementary Table S1. Primer sequences for transcript analysis. Supplementary Figure S1. Gating strategy for identification of monocyte subpopulations. Supplementary Figure S2. CD40 agonist induces accumulation of resident macrophages in spleen. Supplementary Figure S3. Impact of anti-CD40 treatment on Ly6G+ cells within PDAC tumors of KPC mice. Supplementary Figure S4. Strategy for depletion of resident and inflammatory monocyte populations in vivo. Supplementary Figure S5. Effect of clodronate encapsulated liposome (CEL) treatment on peripheral blood myeloid cells. Supplementary Figure S6. Specificity of Ly6C depleting antibody, Monts-1. Supplementary Figure S7. CCL2 regulates CD40-dependent Ly6C+ myeloid cell recruitment to PDAC tumors in KPC mice. Supplementary Figure S8. Anti-CD40 treatment induces systemic cytokine release in mice and humans. Supplementary Figure S9. STAT1 signaling in human monocytes induced by plasma from PDAC patient treated with CP-870,893. Supplementary Figure S10. Anti-fibrotic activity induced with a CD40 agonist is dependent on IFN-gamma. Supplementary Figure S11. CD40 activation does not alter extracellular matrix production or FAP+ fibroblast proliferation. Supplementary Figure S12. Anti-CD40 treatment selectively depletes extracellular matrix proteins within the tumor microenvironment. Supplementary Figure S13. Implantable tumor model of PDAC that reproduces tumor microenvironment of KPC model of spontaneous PDAC. Supplementary Figure S14. Development of an implantable model of PDAC for evaluating monocyte-dependent degradation of cancer fibrosis. Supplementary Figure S15. Gene expression of extracellular matrix and adhesion molecules within the tumor microenvironment in response to anti-CD40 treatment. Supplementary Figure S16. IFN-gamma induces Mmp13 expression in myeloid cells. Supplementary Figure S17. RNA in situ hybridization (ISH) for MMP13 in PDAC tumors. Supplementary Figure S18. Detection of MMP activity in cellular subsets within the tumor microenvironment. Supplementary Figure S19. Protein expression of MMP13 and MMP14 within the tumor microenvironment of spontaneously arising pancreatic tumors in the KPC model. Supplementary Figure S20. Gene expression of Mmp2 and Mmp14 within the tumor microenvironment of pancreatic tumors. Supplementary Figure S21. Anti-fibrotic activity of a CD40 agonist is dependent on MMPs. Supplementary Figure S22. Impact of MMP13 specific inhibitors on CD40 agonist induced collagen degradation. Supplementary Figure S23. Kinetics of anti-CD40 activity on tumor microenvironment. Supplementary Figure S24. Impact of anti-CD40 on CD31+ blood vessel density and vascular patency. Supplementary Figure 25. Anti-CD40 treatment improves gemcitabine efficacy in vivo. Supplementary Figure 26. Anti-CD40 treatment improves gemcitabine efficacy in KPC tumor-bearing mice. Supplementary Figure S27. Impact of MMPs and Ly6C+ cells on anti-tumor activity induced by gemcitabine administered two days after an agonist CD40 antibody. Supplementary Figure S28. Treatment tolerability is dependent on timing of gemcitabine administration after anti-CD40 treatment.</p>