Abstract
One of the main mechanisms for avoiding immune response by cancer cells is mediated by inducing an immunosuppressive environment in the tumor following activation of immune checkpoints, i.e. PD-1 or CTLA-4 receptor inhibitors on T lymphocytes. Interaction inhibition between PD-1 or CTLA-4 and their ligands (PD-L1, CD80, and CD85) leads to unblocking of the T-lymphocyte function, and thus destroys cancer cells. Certain intracellular signaling pathways are also involved in the development of tumor cell immunoresistance. Immunosuppressive pathways' activation blocking may increase the immunological anti-tumor control.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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B7-H1 Antigen / antagonists & inhibitors
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B7-H1 Antigen / metabolism*
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CTLA-4 Antigen / antagonists & inhibitors
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CTLA-4 Antigen / metabolism*
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Female
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Humans
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Immune Tolerance
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Lymphocyte Activation / drug effects
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Male
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Molecular Targeted Therapy / methods
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Programmed Cell Death 1 Receptor / antagonists & inhibitors
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Programmed Cell Death 1 Receptor / metabolism*
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Signal Transduction / drug effects
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T-Lymphocytes, Regulatory / immunology*
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Tumor Escape*
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Tumor Microenvironment / immunology*
Substances
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Antineoplastic Agents
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B7-H1 Antigen
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CD274 protein, human
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CTLA-4 Antigen
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CTLA4 protein, human
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PDCD1 protein, human
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Programmed Cell Death 1 Receptor