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Journal ArticleDOI

TOX promotes the exhaustion of antitumor CD8+ T cells by preventing PD1 degradation in hepatocellular carcinoma.

TLDR
Downregulating TOX expression improves the antitumor function of CD8+ T cells, which shows synergetic role with anti-PD1 therapy, highlighting a promising strategy for enhancement of cancer immunotherapy.
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This article is published in Journal of Hepatology.The article was published on 2019-10-01. It has received 175 citations till now. The article focuses on the topics: T cell & Cytotoxic T cell.

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Citations
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Journal ArticleDOI

Turning Cold into Hot: Firing up the Tumor Microenvironment.

TL;DR: How innate immune sensing machinery, genetic alterations of oncogenic signaling, cellular metabolism, and epigenetic factors are involved in modulating the TME are discussed.
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Immune checkpoint signaling and cancer immunotherapy.

TL;DR: Regulation of immune checkpoint signaling at multiple levels is discussed to provide an overview of the current understanding of checkpoint biology and includes the regulation of surface expression levels for known immune checkpoint proteins via surface delivery, internalization, recycling, and degradation.
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Cancer cell-derived exosomal circUHRF1 induces natural killer cell exhaustion and may cause resistance to anti-PD1 therapy in hepatocellular carcinoma

TL;DR: The expression of circUHRF1 is higher in human HCC tissues than in matched adjacent nontumor tissues and may drive resistance to anti-PD1 immunotherapy in HCC patients, indicating poor clinical prognosis and NK cell dysfunction in patients with HCC.
References
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Journal ArticleDOI

PD-1 and its ligands in tolerance and immunity

TL;DR: Current understanding of the immunoregulatory functions of PD-1 and its ligands and their therapeutic potential are discussed and an inhibitory bidirectional interaction between PD-L1 and B7-1 is discovered, revealing new ways the B7:CD28 family regulates T cell activation and tolerance.
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Cancer immunotherapy using checkpoint blockade

TL;DR: New-generation combinatorial therapies may overcome resistance mechanisms to immune checkpoint therapy, and evidence points to alterations that converge on the antigen presentation and interferon-γ signaling pathways.
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T cell exhaustion

TL;DR: Advances in the molecular delineation of T cell exhaustion are clarifying the underlying causes of this state of differentiation and also suggest promising therapeutic opportunities.
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Molecular and cellular insights into T cell exhaustion

TL;DR: Recent advances that provide a clearer molecular understanding of T cell exhaustion are reviewed and reveal new therapeutic targets for persisting infections and cancer.
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Fundamental Mechanisms of Immune Checkpoint Blockade Therapy

TL;DR: The current state of understanding of T-cell costimulatory mechanisms and checkpoint blockade, primarily of CTLA4 and PD-1, is reviewed, and conceptual gaps in knowledge are highlighted.
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