Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignant tumor in the world and its incidence is increasing in many countries. In recent years, with the deepening understanding of the immune and pathological mechanisms of HCC, immunotherapy based on the regulation of tumor immune microenvironment has become a new treatment choice for patients with HCC. Immune checkpoint inhibitors (ICIs) targeting programmed death protein-1, programmed death protein-ligand-1, or cytotoxic T-lymphocyte-associated antigen 4 are the most widely used. Instead of general immune-enhancing therapies, ICIs can reactivate anti-tumor immune responses by disrupting co-inhibitory T cell signaling. In this review, the research progress and existing problems of ICIs in the treatment of HCC in recent years are reviewed.
Highlights
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world [1]
HCC is a malignant tumor with complex pathogenesis, immunogenicity and high heterogeneity [106]
All authors have read and approved the final version to be published
Summary
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world [1]. PD-L1 formed on the surface of HCC cells can bind to PD-1, and bind to B7.1 on dendritic cells (DCs) to prevent the interaction of B7.1/CD28 to inhibit the activation of anti-tumor T cells, thereby evading T encirclement and suppression of cells [20, 21] Farther, there is another immune checkpoint molecule cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) on Tregs, which can bind with CD80 and CD86 on APCs to inhibit the activation of T lymphocytes, leading to immune escape of HCC cells [22]. There is another immune checkpoint molecule cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) on Tregs, which can bind with CD80 and CD86 on APCs to inhibit the activation of T lymphocytes, leading to immune escape of HCC cells [22] Because of this unique immune tolerance mechanism of liver that forms a highly immunosuppressive microenvironment, the efficacy of traditional drugs is limited [23]. The objective response rate (ORR) of patients with CTLA-4 mAb monotherapy was low [43], so the combination of CTLA-4 mAb with other therapeutic methods
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