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. 2024 Dec 10;13:RP92672. doi: 10.7554/eLife.92672

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© 2024, Go, Demetriou, Valenzano et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 7. — (A) Tissue-resident natural killer (trNK) cell (NK_C1) signature and overall survival in pancreatic ductal adenocarcinoma (PDAC) using the CPTAC3 dataset. (B) Schematic overview of proposed mode of action of CCL5 gradients: CCL5 leads to the recruitment of CCR5⁺ immune cells, including regulatory T-cells (Tregs). Blockade of the CCL5-CCR5 axis, however by CCR5 antagonists, allows recruitment of trNK cells via CCL5-CCR1 signaling while Tregs recruited into the microenvironment are killed off via FasL-mediated trNK killing.

Figure 7—figure supplement 1. — (A) Tissue-resident natural killer (trNK) cell (NK_C1) signature and overall survival in pancreatic ductal adenocarcinoma (PDAC) using the CPTAC3 dataset. (B) Schematic overview of proposed mode of action of CCL5 gradients: CCL5 leads to the recruitment of CCR5⁺ immune cells, including regulatory T-cells (Tregs). Blockade of the CCL5-CCR5 axis, however by CCR5 antagonists, allows recruitment of trNK cells via CCL5-CCR1 signaling while Tregs recruited into the microenvironment are killed off via FasL-mediated trNK killing.