Dendritic cell redundancy enables priming of anti-tumor CD4 T cells in pancreatic cancer
Pancreatic ductal adenocarcinoma (PDAC) is resistant to current immunotherapies. Using mouse models, we achieved durable remissions and immunological memory after administration of anti-CTLA-4 and anti-PD-1. The mechanism of action involves activation of cDC2 cells and CD4 T cells. To validate these findings in humans, we collected tumor samples from patients with pancreatic cancer. We performed single-cell RNA-seq analyses to assess the abundance of cDC2 cells before and after treatment. This dataset consists of Illumina NovaSeq sequencing output (FASTQ files) from blood and tumor libraries prepared using the 10x Genomics Single Cell 5' Immune Profiling kit. FASTQ files are provided for gene expression (GEX), TCR, and, for multiplexed samples, HTO libraries.