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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Gastroenterology. 2013 Jun;144(6):1199–209.e4. doi: 10.1053/j.gastro.2013.02.007

Figure 2.

Figure 2

Inflammation in PDAC. Activation of Kras in pancreatic epithelial cells promotes production of inflammatory mediators (including IL-6 and IL-11, which activate STAT3 in an autocrine manner) or recruits myeloid cells that produce IL-6 and sIL-6R to activate STAT3 in a paracrine manner. NF-κB also can be activated in an autocrine or paracrine manner by TNFα and IL-1α, creating a positive-feedback loop to maintain the tumor’s inflammatory microenvironment. Inflammation-induced activation of STAT3 and NF-κB promotes cell survival, proliferation, and the EMT, which contribute to initiation and progression of PDAC. Pancreatic neoplastic cells that express oncogenic Kras also produce the inflammatory cytokine granulocyte-macrophage colony–stimulating factor (GM-CSF), leading to recruitment of myeloid progenitor cells and their subsequent differentiation into MDSCs, which suppress the immune surveillance function of CD8+ T cells. COX2, cyclooxygenase 2; MMP, matrix metalloproteinase.