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McAllister, Florencia; Bailey, Jennifer M.; Alsina, Janivette; Nirschl, Christopher J.; Sharma, Rajni; Fan, Hongni; Rattigan, Yanique; Roeser, Jeffrey C.; Lankapalli, Rachana H.; Zhang, Hao; Jaffee, Elizabeth M.; Drake, Charles G.; Housseau, Franck; Maitra, Anirban; Kolls, Jay K.; Sears, Cynthia L.; Pardoll, Drew M.; Leach, Steven D.
Cancer cell, 05/2014, Volume: 25, Issue: 5Journal Article
Many human cancers are dramatically accelerated by chronic inflammation. However, the specific cellular and molecular elements mediating this effect remain largely unknown. Using a murine model of pancreatic intraepithelial neoplasia (PanIN), we found that KrasG12D induces expression of functional IL-17 receptors on PanIN epithelial cells and also stimulates infiltration of the pancreatic stroma by IL-17-producing immune cells. Both effects are augmented by associated chronic pancreatitis, resulting in functional in vivo changes in PanIN epithelial gene expression. Forced IL-17 overexpression dramatically accelerates PanIN initiation and progression, while inhibition of IL-17 signaling using genetic or pharmacologic techniques effectively prevents PanIN formation. Together, these studies suggest that a hematopoietic-to-epithelial IL-17 signaling axis is a potent and requisite driver of PanIN formation. Display omitted •IL-17+ T cells are recruited to the pancreas in response to Kras and inflammation•IL-17A overexpression accelerates PanIN initiation and progression•Inhibition of IL-17 signaling effectively prevents PanIN initiation and progression•Kras activates expression of functional IL-17 receptors on PanIN epithelium McAllister et al. show that KrasG12D induces IL-17 receptors expression on PanIN epithelial cells and stimulates infiltration of IL-17-producing immune cells in a murine PanIN model, the latter of which is confirmed in human PanIN and that inhibition of IL-17 signaling prevents pancreatic neoplasia initiation.
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