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However, poor cancer-specificity of chemotherapeutic drugs can induce systemic toxicities as well as bone marrow suppression and damage to the host immune system, resulting in serious side effects and low response rate of patients 8. These cascade events of ICD turn the immunosuppressive tumor microenvironment (ITM) to the immune-responsive tumors, leading to increase the ICB immunotherapy efficiency 6, 7. The underlying mechanism is that dying cells by ICD-inducing chemotherapeutic drugs release damage-associated molecular patterns (DAMPs) to promote the cross-presentation of tumor-associated antigens to the dendritic cells (DCs), and thus provokes DC maturation and T lymphocyte infiltration 3 - 6. Furthermore, the therapeutic outcomes of ICB immunotherapy have dramatically improved when combined with immunogenic cell death (ICD)-inducing chemotherapeutic drugs in pre-clinical and clinical studies 2. Immune checkpoint blockade (ICB) immunotherapy has provided significant clinical advances to combat a variety of cancers, which provokes an antitumor immune response via monoclonal antibodies (mAbs) against programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1) or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) 1. In tumor models, PD-NPs accumulate within tumor tissues via enhanced permeability and retention (EPR) effect and induce immune-responsive tumors by recruiting a large amount of immune cells.Ĭonclusions: Collectively, targeted tumor delivery of anti-PD-L1 peptide and DOX via PD-NPs efficiently inhibit tumor progression with minimal side effects. Concurrently, PD-L1 blockade by PD-NPs disrupt the immune-suppressing pathway of cancer cells, resulting in proliferation and reinvigoration of T lymphocytes. Results: The PD-NPs are taken up by PD-L1 receptor-mediated endocytosis and then induce ICD in cancer cells by DOX release. The antitumor efficacy and immune responses with minimal side effects by PD-NPs combining PD-L1 blockade and ICD are evaluated in breast tumor models. Methods: The functional peptide, consisted of anti-PD-L1 peptide and cathepsin B-specific cleavable peptide, is conjugated to a doxorubicin (DOX), resulting in prodrug nanoparticles of PD-NPs via intermolecular interactions. In this study, we propose anti-PD-L1 peptide-conjugated prodrug nanoparticles (PD-NPs) to overcome these obstacles of current cancer immunotherapy. However, such combination therapeutic regimen has suffered from severe toxicity of both drugs and low response rate of patients.

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These infections might corrupt your computer installation or breach your privacy.Īutomatic data processing keygen or key generator might contain a trojan horse opening a backdoor on your computer.Rationale: Cancer immunotherapy combining immune checkpoint blockade (ICB) with chemotherapeutic drugs has provided significant clinical advances.

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