STING agonist inflames the pancreatic cancer immune microenvironment and reduces tumor burden in mouse models

Weiqing Jing, Donna McAllister, Emily P. Vonderhaar, Katie Palen, Matthew J. Riese, Jill Gershan, Bryon D. Johnson, Michael B. Dwinell*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

65 Scopus citations


Pancreatic cancer is characterized by an immune suppressive stromal reaction that creates a barrier to therapy. A murine transgenic pancreatic cancer cell line that recapitulates human disease was used to test whether a STimulator of Interferon Genes (STING) agonist could reignite immunologically inert pancreatic tumors. STING agonist treatment potently changed the tumor architecture, altered the immune profile, and increased the survival of tumor-bearing mice. Notably, STING agonist increased numbers and activity of cytotoxic T cells within tumors and decreased levels of suppressive regulatory T cells. Further, STING agonist treatment upregulated costimulatory molecule expression on cross-presenting dendritic cells and reprogrammed immune-suppressive macrophages into immune-activating subtypes. STING agonist promoted the coordinated and differential cytokine production by dendritic cells, macrophages, and pancreatic cancer cells. Cumulatively, these data demonstrate that pancreatic cancer progression is potently inhibited by STING agonist, which reignited immunologically cold pancreatic tumors to promote trafficking and activation of tumor-killing T cells.

Original languageEnglish (US)
Article number115
JournalJournal for immunotherapy of cancer
Issue number1
StatePublished - Apr 29 2019


  • CXCL10
  • Cancer proliferation
  • Cytotoxic T cells
  • Immune activation
  • STING agonist
  • Tumor infiltrating lymphocytes
  • Tumor selectivity

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Cancer Research
  • Immunology and Allergy
  • Pharmacology
  • Immunology


Dive into the research topics of 'STING agonist inflames the pancreatic cancer immune microenvironment and reduces tumor burden in mouse models'. Together they form a unique fingerprint.

Cite this