Abstract
Tumor cells can evade immune surveillance through overexpressing the ligands of checkpoint receptors on tumor cells or adjacent cells, leading T cells to anergy or exhaustion. Growing evidence of the interaction between tumor cells and microenvironment promoted the emergence of immune-checkpoint blockade. By targeting programmed cell death-1 (PD-1) pathway, cytotoxic activity of T cell is enhanced significantly and tumor cell lysis is induced subsequently. Currently, various antibodies against PD-1 and programmed death-ligand 1 (PD-L1) are under clinical studies in lymphomas. In this review, we outline the rationale for investigation of PD-1-PD-L1 immune-checkpoint blockade in lymphomas and discuss their prospect of applications in clinical treatment.
Keywords:
Immune checkpoint; Lymphoma; Nivolumab; PD-1; PD-L1; Pembrolizumab.
MeSH terms
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Antibodies, Monoclonal / therapeutic use
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Antibodies, Monoclonal, Humanized / therapeutic use
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Antineoplastic Agents / therapeutic use*
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B7-H1 Antigen / antagonists & inhibitors
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B7-H1 Antigen / genetics
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B7-H1 Antigen / immunology*
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Clinical Trials as Topic
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Clonal Anergy / genetics
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Cytotoxicity, Immunologic / drug effects
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Gene Expression Regulation, Neoplastic*
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Humans
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Lymphoma / drug therapy*
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Lymphoma / genetics
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Lymphoma / immunology
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Lymphoma / pathology
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Nivolumab
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Programmed Cell Death 1 Receptor / antagonists & inhibitors
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Programmed Cell Death 1 Receptor / genetics
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Programmed Cell Death 1 Receptor / immunology*
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Signal Transduction
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T-Lymphocytes / drug effects*
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T-Lymphocytes / immunology
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T-Lymphocytes / pathology
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Tumor Escape
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Tumor Microenvironment / genetics
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Tumor Microenvironment / immunology
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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B7-H1 Antigen
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CD274 protein, human
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PDCD1 protein, human
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Programmed Cell Death 1 Receptor
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Nivolumab
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pembrolizumab