Abstract
T-cell exhaustion was originally identified during chronic infection in mice, and was subsequently observed in humans with cancer. The exhausted T cells in the tumor microenvironment show overexpressed inhibitory receptors, decreased effector cytokine production and cytolytic activity, leading to the failure of cancer elimination. Restoring exhausted T cells represents an inspiring strategy for cancer treatment, which has yielded promising results and become a significant breakthrough in the cancer immunotherapy. In this review, we overview the updated understanding on the exhausted T cells in cancer and their potential regulatory mechanisms and discuss current therapeutic interventions targeting exhausted T cells in clinical trials.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Basic-Leucine Zipper Transcription Factors / metabolism
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Cytokines / metabolism
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Humans
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Lymphocyte Activation / immunology
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Mice
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NFATC Transcription Factors / metabolism
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Neoplasms / immunology*
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Positive Regulatory Domain I-Binding Factor 1
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Programmed Cell Death 1 Receptor / genetics
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Programmed Cell Death 1 Receptor / metabolism
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Repressor Proteins / metabolism
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T-Box Domain Proteins / metabolism
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T-Lymphocytes / immunology*
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Tumor Escape / immunology*
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Tumor Microenvironment / immunology*
Substances
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BATF protein, human
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Basic-Leucine Zipper Transcription Factors
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Cytokines
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NFATC Transcription Factors
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NFATC1 protein, human
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PDCD1 protein, human
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Programmed Cell Death 1 Receptor
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Repressor Proteins
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T-Box Domain Proteins
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T-box transcription factor TBX21
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PRDM1 protein, human
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Positive Regulatory Domain I-Binding Factor 1