Preferential activation of type I interferon-mediated antitumor inflammatory signaling by CuS/MnO/diAMP nanoparticles enhances anti-PD-1 therapy for sporadic colorectal cancer.

Converting the "cold" tumor microenvironment (TME) to a "hot" milieu has become the prevailing approach for enhancing the response of immune-excluded/immunosuppressed colorectal cancer (CRC) patients to immune checkpoint blockade (ICB) therapy. During this process, inflammation accompanied by different kinds of chemokines/cytokines inevitably occurs. However, some activated inflammatory signals exhibit protumor potency.