fig1

Figure 1. Under the action of DDRis, tumor cells release interferon, and chemotactic substances act as signals to immune cells to promote immune recognition and tumor killing by increasing the immunogenicity of the tumor and recruiting T cells. PD-1 is upregulated at the transcriptional level to activate T cells, and negative costimulatory signals transmitted by PD-1 upon binding to its ligands inhibit T lymphocyte proliferation. In the tumor microenvironment, antitumor immune responses can be maintained by blocking the connection of PD-1 to PD-L1 expressed on tumor or mesenchymal cells.