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  1. Artikel: Intracellular K

    Collier, Camille / Wucherer, Kelly / McWhorter, Matthew / Jenkins, Chelsea / Bartlett, Alexandra / Roychoudhuri, Rahul / Eil, Robert

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The cancer-killing activity of T cells is often compromised within tumors, allowing disease progression. We previously found that intratumoral elevations in extracellular K : Synopsis: High extracellular ... ...

    Abstract The cancer-killing activity of T cells is often compromised within tumors, allowing disease progression. We previously found that intratumoral elevations in extracellular K
    Synopsis: High extracellular K
    Sprache Englisch
    Erscheinungsdatum 2023-09-15
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.09.13.556997
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Intracellular K+ Limits T-cell Exhaustion and Preserves Antitumor Function.

    Collier, Camille / Wucherer, Kelly / McWhorter, Matthew / Jenkins, Chelsea / Bartlett, Alexandra / Roychoudhuri, Rahul / Eil, Robert

    Cancer immunology research

    2023  Band 12, Heft 1, Seite(n) 36–47

    Abstract: T cells are often compromised within cancers, allowing disease progression. We previously found that intratumoral elevations in extracellular K+, related to ongoing cell death, constrained CD8+ T-cell Akt-mTOR signaling and effector function. To ... ...

    Abstract T cells are often compromised within cancers, allowing disease progression. We previously found that intratumoral elevations in extracellular K+, related to ongoing cell death, constrained CD8+ T-cell Akt-mTOR signaling and effector function. To alleviate K+-mediated T-cell dysfunction, we pursued genetic means to lower intracellular K+. CD8+ T cells robustly and dynamically express the Na+/K+ ATPase, among other K+ transporters. CRISPR-Cas9-mediated disruption of the Atp1a1 locus lowered intracellular K+ and elevated the resting membrane potential (i.e., Vm, Ψ). Despite compromised Ca2+ influx, Atp1a1-deficient T cells harbored tonic hyperactivity in multiple signal transduction cascades, along with a phenotype of exhaustion in mouse and human CD8+ T cells. Provision of exogenous K+ restored intracellular levels in Atp1a1-deficient T cells and prevented damaging levels of reactive oxygen species (ROS), and both antioxidant treatment and exogenous K+ prevented Atp1a1-deficient T-cell exhaustion in vitro. T cells lacking Atp1a1 had compromised persistence and antitumor activity in a syngeneic model of orthotopic murine melanoma. Translational application of these findings will require balancing the beneficial aspects of intracellular K+ with the ROS-dependent nature of T-cell effector function. See related Spotlight by Banuelos and Borges da Silva, p. 6.
    Mesh-Begriff(e) Humans ; Animals ; Mice ; Reactive Oxygen Species/metabolism ; T-Cell Exhaustion ; Signal Transduction/genetics ; Sodium-Potassium-Exchanging ATPase/genetics ; Sodium-Potassium-Exchanging ATPase/metabolism ; CD8-Positive T-Lymphocytes/metabolism
    Chemische Substanzen Reactive Oxygen Species ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
    Sprache Englisch
    Erscheinungsdatum 2023-12-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2732489-8
    ISSN 2326-6074 ; 2326-6066
    ISSN (online) 2326-6074
    ISSN 2326-6066
    DOI 10.1158/2326-6066.CIR-23-0319
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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