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The drivers and the specification of CD4 +  T cell differentiation in the tumor microenvironment and their contributions to tumor immunity or tolerance are incompletely understood. Using models of pancreatic ductal adenocarcinoma (PDA), we show that a distinct subset of tumor-infiltrating dendritic cells (DC) promotes PDA growth by directing a unique T H -program. Specifically, CD11b + CD103 −  DC predominate in PDA, express high IL-23 and TGF-β, and induce FoxP3  neg   tumor-promoting IL-10 + IL-17 + IFNγ +  regulatory CD4 +  T cells. The balance between this distinctive T H  program and canonical FoxP3 +  T REGS  is unaffected by pattern recognition receptor ligation and is modulated by DC expression of retinoic acid. This T H -signature is mimicked in human PDA where it is associated with immune-tolerance and diminished patient survival. Our data suggest that CD11b + CD103 −  DC promote CD4 +  T cell tolerance in PDA which may underscore its resistance to immunotherapy.

Specialized dendritic cells induce tumor-promoting IL-10+IL-17+ FoxP3neg regulatory CD4+ T cells in pancreatic carcinoma