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- W4308709478 abstract "Summary Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy resistant to immunotherapy. The pancreatic tumor microenvironment is shaped and maintained by myeloid cells that outnumber tumor cells. Here, using monocyte fate-mapping PDA mouse models and human tumor tissues, we identify monocytes give rise to most heterogeneous macrophage subpopulations in PDA. We show that monocyte differentiation is governed by the local presence of CD4, but not CD8, T cells. We demonstrate that tumor specific CD4 T cells induce monocyte differentiation into antitumor MHCII hi proinflammatory macrophages dependent on non-redundant IFNγ and CD40 signaling pathways that suppress tumor growth. Pancreatic tissue-resident macrophages exhibit an immunosuppressive pro-tumor state that is refractory to the modulatory effects of antitumor CD4 T cells. Intratumoral monocytes adopt a pro-tumor fate indistinguishable from tissue-resident macrophages following CD4 T cell depletion. Thus, tumor-specific CD4 T cell governance of monocyte fate promotes immune-mediated control of solid tumors. Highlights ▪ Circulating monocytes are progenitors to most heterogeneous macrophage subsets in PDA ▪ Monocyte-derived macrophage acquisition of an MHCII hi phenotype is dependent on tumor-specific CD4 T cells ▪ In the absence of CD4 T cells, monocyte-derived macrophages acquire tissue resident macrophage traits and tumors rapidly progress ▪ IFNγ and CD40 signaling are nonredundant and critical determinants of intratumoral monocyte fate" @default.
- W4308709478 created "2022-11-14" @default.
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- W4308709478 date "2022-11-10" @default.
- W4308709478 modified "2023-09-27" @default.
- W4308709478 title "Tumor-specific CD4 T cells instruct monocyte differentiation in pancreatic ductal adenocarcinoma" @default.
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- W4308709478 doi "https://doi.org/10.1101/2022.11.09.515858" @default.
- W4308709478 hasPublicationYear "2022" @default.
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