![]() ![]() T cells in particular have been widely studied regarding their role in PDAC progression. Importantly, many of the immune cells within the TME are immunosuppressive while immunosupportive cells are either excluded or reprogrammed. Many studies have explored the immune cell infiltrate and how its composition affects PDAC patient outcomes and survival. ![]() The PDAC TME is marked by a fibrotic stroma which contains an array of immune cells. Significance of the Inflammatory Immune Infiltrate in PDAC ![]() Finally, we describe a cadre of treatment targets, including those intended to overcome TAM and TAN recruitment and function, to circumvent barriers presented by immune infiltration in pancreatic adenocarcinoma.ΔΆ. We also discuss immune mechanisms driving resistance to standard of care modalities. The sequelae of macrophage and neutrophil activities contributes to tumor remodeling, fibrosis, hypoxia, and progression. We narrow in on tumor macrophage (TAM) spatial arrangement, polarity/function, recruitment, and origin to introduce a concept where interactions with tumor neutrophils (TAN) perpetuate the microenvironment. Here, we emphasize how immune cell interactions generate tumor progression and treatment resistance. In this review, we discuss the immune composition of pancreatic tumors, including the counterintuitive fact that there is a significant inflammatory immune infiltrate in pancreatic cancer yet anti-tumor mechanisms are subverted and immune behaviors are suppressed. Uncovering innovative therapeutic modalities to target the resistance mechanisms that make pancreatic cancer largely incurable are urgently needed. These poor outcomes are driven by failure of early detection, treatment resistance, and propensity for early metastatic spread. Despite modest improvements in survival in recent years, pancreatic adenocarcinoma remains a deadly disease with a 5-year survival rate of only 9%. ![]()
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