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Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.12 Figure 2 Inflammatory macrophage-driven signalling leading to acinar-to-ductal metaplasia Figure 2 | Inflammatory macrophage-driven signalling leading to acinar-to-ductal metaplasia. Inflammatory macrophages can initiate acinar-to-ductal metaplasia (ADM) through NF-κB activation as caused by secreted inflammatory cytokines such as TNF and the chemokine CCL5. Macrophage-secreted IL-6 contributes to ADM and the development of PDAC through JAK–STAT3 signalling. In addition, macrophage-secreted matrix metalloproteinases (MMPs) contribute to extracellular matrix (ECM) degradation and activate Notch signalling (NICD, Notch intracellular domain). Other transcription factors activated in acinar cells after inflammation and contributing to ADM are NFATC1 and NFATC4. Storz, P. (2017) Acinar cell plasticity and development of pancreatic ductal adenocarcinoma Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.12