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  1. Article ; Online: Tumor microenvironmental signals reshape chromatin landscapes to limit the functional potential of exhausted T cells.

    Ford, B Rhodes / Vignali, Paolo D A / Rittenhouse, Natalie L / Scharping, Nicole E / Peralta, Ronal / Lontos, Konstantinos / Frisch, Andrew T / Delgoffe, Greg M / Poholek, Amanda C

    Science immunology

    2022  Volume 7, Issue 74, Page(s) eabj9123

    Abstract: Response rates to immunotherapy in solid tumors remain low due in part to the elevated prevalence of terminally exhausted T cells, a hypofunctional differentiation state induced through persistent antigen and stress signaling. However, the mechanisms ... ...

    Abstract Response rates to immunotherapy in solid tumors remain low due in part to the elevated prevalence of terminally exhausted T cells, a hypofunctional differentiation state induced through persistent antigen and stress signaling. However, the mechanisms promoting progression to terminal exhaustion in the tumor remain undefined. Using the low-input chromatin immunoprecipitation sequencing method CUT&RUN, we profiled the histone modification landscape of tumor-infiltrating CD8
    MeSH term(s) CD8-Positive T-Lymphocytes ; Chromatin/metabolism ; Histones/metabolism ; Humans ; Hypoxia/metabolism ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Neoplasms ; Tumor Microenvironment
    Chemical Substances Chromatin ; Histones ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; KDM6B protein, human (EC 1.14.11.-)
    Language English
    Publishing date 2022-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abj9123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Metabolic reprogramming via an engineered PGC-1α improves human chimeric antigen receptor T-cell therapy against solid tumors.

    Lontos, Konstantinos / Wang, Yiyang / Joshi, Supriya K / Frisch, Andrew T / Watson, McLane J / Kumar, Alok / Menk, Ashley V / Wang, Yupeng / Cumberland, Rachel / Lohmueller, Jason / Carrizosa, Esteban / Boyerinas, Benjamin / Delgoffe, Greg M

    Journal for immunotherapy of cancer

    2022  Volume 11, Issue 3

    Abstract: Background: Cellular immunotherapies for cancer represent a means by which a patient's immune system can be augmented with high numbers of tumor-specific T cells. Chimeric antigen receptor (CAR) therapy involves genetic engineering to 'redirect' ... ...

    Abstract Background: Cellular immunotherapies for cancer represent a means by which a patient's immune system can be augmented with high numbers of tumor-specific T cells. Chimeric antigen receptor (CAR) therapy involves genetic engineering to 'redirect' peripheral T cells to tumor targets, showing remarkable potency in blood cancers. However, due to several resistance mechanisms, CAR-T cell therapies remain ineffective in solid tumors. We and others have shown the tumor microenvironment harbors a distinct metabolic landscape that produces a barrier to immune cell function. Further, altered differentiation of T cells within tumors induces defects in mitochondrial biogenesis, resulting in severe cell-intrinsic metabolic deficiencies. While we and others have shown murine T cell receptor (TCR)-transgenic cells can be improved through enhanced mitochondrial biogenesis, we sought to determine whether human CAR-T cells could be enabled through a metabolic reprogramming approach.
    Materials and methods: Anti-EGFR CAR-T cells were infused in NSG mice which bore A549 tumors. The tumor infiltrating lymphocytes were analyzed for exhaustion and metabolic deficiencies. Lentiviruses carrying PPAR-gamma coactivator 1α (PGC-1α), PGC-1α
    Results: Here, in this study, we show that an inhibition resistant, engineered version of PGC-1α, can metabolically reprogram human CAR-T cells. Transcriptomic profiling of PGC-1α-transduced CAR-T cells showed this approach effectively induced mitochondrial biogenesis, but also upregulated programs associated with effector functions. Treatment of immunodeficient animals bearing human solid tumors with these cells resulted in substantially improved in vivo efficacy. In contrast, a truncated version of PGC-1α, NT-PGC-1α, did not improve the in vivo outcomes.
    Conclusions: Our data further support a role for metabolic reprogramming in immunomodulatory treatments and highlight the utility of genes like PGC-1α as attractive candidates to include in cargo along with chimeric receptors or TCRs for cell therapy of solid tumors.
    MeSH term(s) Humans ; Animals ; Mice ; Receptors, Chimeric Antigen ; Immunotherapy, Adoptive/methods ; Neoplasms ; Receptors, Antigen, T-Cell ; T-Lymphocytes ; Tumor Microenvironment
    Chemical Substances Receptors, Chimeric Antigen ; Receptors, Antigen, T-Cell
    Language English
    Publishing date 2022-10-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2719863-7
    ISSN 2051-1426 ; 2051-1426
    ISSN (online) 2051-1426
    ISSN 2051-1426
    DOI 10.1136/jitc-2022-006522
    Database MEDical Literature Analysis and Retrieval System OnLINE

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