作者: Constantinos P. Zambirinis , Elliot Levie , Susanna Nguy , Antonina Avanzi , Rocky Barilla
DOI: 10.1084/JEM.20142162
关键词:
摘要: Modulation of Toll-like receptor (TLR) signaling can have protective or protumorigenic effects on oncogenesis depending the cancer subtype and specific inflammatory elements within tumor milieu. We found that TLR9 is widely expressed early during course pancreatic transformation ligands are ubiquitous microenvironment. ligation markedly accelerates oncogenesis, whereas deletion protective. show activation has distinct epithelial, inflammatory, fibrogenic cellular subsets in carcinoma plays a central role cross talk between these compartments. Specifically, induce proinflammatory transformed epithelial cells, but does not elicit oncogene expression cell proliferation. Conversely, induces stellate cells (PSCs) to become secrete chemokines promote TLR9-activated PSCs mediate their compartment via CCL11. Additionally, immune-suppressive microenvironment (TME) induction regulatory T recruitment myeloid-derived suppressor Collectively, our work shows which from its influence extrapancreatic malignancies mechanistic other TLRs oncogenesis.