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. 2021 Sep 3;9(9):e002876. doi: 10.1136/jitc-2021-002876

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Schematic representation of IMO-2125 mechanism of action. IMO-2125 (intratumoral) treatment leads to dendritic cell migration in draining lymph nodes of all pancreatic ductal adenocarcinoma, whereas only in the high immunological potential tumors the expression of IFNγ determines a cytokines storm that exacerbates the IMO-2125 antitumor effect. The expansion and activation of T cells in tumor-draining lymph nodes occur for all IMO-2125-treated tumors. Whereas in tumor with high immunological potential, T cells are able to efficiently kill cancer cells, tumors with low or no immunological potential are able to escape to T lymphocytes through an increase of autophagy flux and expression of immune suppressive cytokines that limited efficacy of IMO-2125. Anti-PD1 treatment is able to increase the efficacy of IMO-2125, potentiating the infiltration of T cells, only in tumor with high and low immunological potential, while no effect in the extremely refractory tumors is evident.