| First Author | Hegde S | Year | 2020 |
| Journal | Cancer Cell | Volume | 37 |
| Issue | 3 | Pages | 289-307.e9 |
| PubMed ID | 32183949 | Mgi Jnum | J:285844 |
| Mgi Id | MGI:6400700 | Doi | 10.1016/j.ccell.2020.02.008 |
| Citation | Hegde S, et al. (2020) Dendritic Cell Paucity Leads to Dysfunctional Immune Surveillance in Pancreatic Cancer. Cancer Cell 37(3):289-307.e9 |
| abstractText | Here, we utilized spontaneous models of pancreatic and lung cancer to examine how neoantigenicity shapes tumor immunity and progression. As expected, neoantigen expression during lung adenocarcinoma development leads to T cell-mediated immunity and disease restraint. By contrast, neoantigen expression in pancreatic ductal adenocarcinoma (PDAC) results in exacerbation of a fibro-inflammatory microenvironment that drives disease progression and metastasis. Pathogenic TH17 responses are responsible for this neoantigen-induced tumor progression in PDAC. Underlying these divergent T cell responses in pancreas and lung cancer are differences in infiltrating conventional dendritic cells (cDCs). Overcoming cDC deficiency in early-stage PDAC leads to disease restraint, while restoration of cDC function in advanced PDAC restores tumor-restraining immunity and enhances responsiveness to radiation therapy. |
