Class II transactivator-induced MHC class II expression in pancreatic cancer cells leads to tumor rejection and a specific antitumor memory response.

摘要: OBJECTIVES The loss of major histocompatibility complex (MHC) classes I and II is a well-known mechanism by which cancer cells are able to escape from immune recognition. In this study, we analyzed the expression antigen processing presenting molecules in 2 cell lines derived mouse models pancreatic ductal adenocarcinoma (PDA) effects re-expression MHC class on PDA rejection. METHODS were for I, II, antigen-processing flow cytometry or polymerase chain reaction. We generated stable PDA-MHC transactivator (CIITA) injected them into syngeneic mice. CD4 CD8 T-cell role was vitro vivo. RESULTS Murine negative molecules, but their restored exogenous interferon-γ. CIITA-tumor rejected 80% 100% mice, also developed long-lasting memory. assays immunohistochemical analyses revealed recruitment T effector tumor area. CONCLUSIONS Overall, these data confirm that immunotherapy feasible therapeutic approach recognize target an aggressive such as PDA.