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  1. Book: Metabolism and autophagy in the immune system

    Rathmell, Jeffrey C.

    (Immunological reviews ; 249)

    2012  

    Author's details Jeffrey C. Rathmell, guest ed
    Series title Immunological reviews ; 249
    Collection
    Language English
    Size 275 S. : Ill.
    Publisher Wiley-Blackwell
    Publishing place Oxford
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT017434236
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 160 -249- verfügbar in Königswinter Königswinter

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  2. Article ; Online: Obesity, Immunity, and Cancer.

    Rathmell, Jeffrey C

    The New England journal of medicine

    2021  Volume 384, Issue 12, Page(s) 1160–1162

    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/metabolism ; Dietary Fats/metabolism ; Disease Models, Animal ; Fatty Acids/metabolism ; Humans ; Mice ; Neoplasms/etiology ; Neoplasms/genetics ; Neoplasms/metabolism ; Obesity/complications ; Obesity/immunology ; Obesity/metabolism ; Oxidation-Reduction
    Chemical Substances Dietary Fats ; Fatty Acids
    Language English
    Publishing date 2021-03-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr2035081
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Metabolic programming and immune suppression in the tumor microenvironment.

    Arner, Emily N / Rathmell, Jeffrey C

    Cancer cell

    2023  Volume 41, Issue 3, Page(s) 421–433

    Abstract: Increased glucose metabolism and uptake are characteristic of many tumors and used clinically to diagnose and monitor cancer progression. In addition to cancer cells, the tumor microenvironment (TME) encompasses a wide range of stromal, innate, and ... ...

    Abstract Increased glucose metabolism and uptake are characteristic of many tumors and used clinically to diagnose and monitor cancer progression. In addition to cancer cells, the tumor microenvironment (TME) encompasses a wide range of stromal, innate, and adaptive immune cells. Cooperation and competition between these cell populations supports tumor proliferation, progression, metastasis, and immune evasion. Cellular heterogeneity leads to metabolic heterogeneity because metabolic programs within the tumor are dependent not only on the TME cellular composition but also on cell states, location, and nutrient availability. In addition to driving metabolic plasticity of cancer cells, altered nutrients and signals in the TME can lead to metabolic immune suppression of effector cells and promote regulatory immune cells. Here we discuss how metabolic programming of cells within the TME promotes tumor proliferation, progression, and metastasis. We also discuss how targeting metabolic heterogeneity may offer therapeutic opportunities to overcome immune suppression and augment immunotherapies.
    MeSH term(s) Humans ; Tumor Microenvironment ; Neoplasms/drug therapy ; Immunotherapy ; Lymphocytes/metabolism
    Language English
    Publishing date 2023-02-16
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2023.01.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Immunometabolic Maladaptations to the Tumor Microenvironment.

    Hathaway, Emma S / Jennings, Erin Q / Rathmell, Jeffrey C

    Cold Spring Harbor perspectives in medicine

    2024  

    Abstract: Tumors consist of cancer cells and a wide range of tissue resident and infiltrating cell types. Tumor metabolism, however, has largely been studied on whole tumors or cancer cells and the metabolism of infiltrating immune cells remains poorly understood. ...

    Abstract Tumors consist of cancer cells and a wide range of tissue resident and infiltrating cell types. Tumor metabolism, however, has largely been studied on whole tumors or cancer cells and the metabolism of infiltrating immune cells remains poorly understood. It is now clear from a range of analyses and metabolite rescue studies that metabolic adaptations to the tumor microenvironment (TME) directly impede T-cell and macrophage effector functions. The drivers of metabolic adaptation to the TME and metabolic immune suppression include depletion of essential nutrients, accumulation of waste products or immune suppression metabolites, and metabolic signaling through altered posttranslational modifications. Each infiltrating immune cell subset differs, however, with specific metabolic requirements and adaptations that can be maladaptive for antitumor immunity. Here, we review T-cell and macrophage adaptation and metabolic immune suppression in solid tumors. Ultimately, understanding and addressing these challenges will improve cancer immunotherapy and adoptive chimeric antigen receptor T-cell therapies.
    Language English
    Publishing date 2024-03-04
    Publishing country United States
    Document type Journal Article
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a041547
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Nutrient inputs and social metabolic control of T cell fate.

    Bacigalupa, Zachary A / Landis, Madelyn D / Rathmell, Jeffrey C

    Cell metabolism

    2023  Volume 36, Issue 1, Page(s) 10–20

    Abstract: Cells in multicellular organisms experience diverse neighbors, signals, and evolving physical environments that drive functional and metabolic demands. To maintain proper development and homeostasis while avoiding inappropriate cell proliferation or ... ...

    Abstract Cells in multicellular organisms experience diverse neighbors, signals, and evolving physical environments that drive functional and metabolic demands. To maintain proper development and homeostasis while avoiding inappropriate cell proliferation or death, individual cells interact with their neighbors via "social" cues to share and partition available nutrients. Metabolic signals also contribute to cell fate by providing biochemical links between cell-extrinsic signals and available resources. In addition to metabolic checkpoints that sense nutrients and directly supply molecular intermediates for biosynthetic pathways, many metabolites directly signal or provide the basis for post-translational modifications of target proteins and chromatin. In this review, we survey the landscape of T cell nutrient sensing and metabolic signaling that supports proper immunity while avoiding immunodeficiency or autoimmunity. The integration of cell-extrinsic microenvironmental cues with cell-intrinsic metabolic signaling provides a social metabolic control model to integrate cell signaling, metabolism, and fate.
    MeSH term(s) T-Lymphocytes ; Cell Differentiation ; Chromatin/metabolism ; Signal Transduction ; Nutrients
    Chemical Substances Chromatin
    Language English
    Publishing date 2023-12-19
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2023.12.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Pushing the boundaries with collision collaboration: the marriage of ideas.

    Rathmell, Jeffrey C / Rathmell, W Kimryn

    The Journal of clinical investigation

    2021  Volume 131, Issue 2

    MeSH term(s) Biomedical Research ; COVID-19/epidemiology ; COVID-19/genetics ; COVID-19/metabolism ; Humans ; Interdisciplinary Research ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism
    Language English
    Publishing date 2021-01-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI145964
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  7. Article ; Online: The Complex Integration of T-cell Metabolism and Immunotherapy.

    Madden, Matthew Z / Rathmell, Jeffrey C

    Cancer discovery

    2021  Volume 11, Issue 7, Page(s) 1636–1643

    Abstract: Immune oncology approaches of adoptive cell therapy and immune checkpoint blockade aim to activate T cells to eliminate tumors. Normal stimulation of resting T cells induces metabolic reprogramming from catabolic and oxidative metabolism to aerobic ... ...

    Abstract Immune oncology approaches of adoptive cell therapy and immune checkpoint blockade aim to activate T cells to eliminate tumors. Normal stimulation of resting T cells induces metabolic reprogramming from catabolic and oxidative metabolism to aerobic glycolysis in effector T cells, and back to oxidative metabolism in long-lived memory cells. These metabolic reprogramming events are now appreciated to be essential aspects of T-cell function and fate. Here, we review these transitions, how they are disrupted by T-cell interactions with tumors and the tumor microenvironment, and how they can inform immune oncology to enhance T-cell function against tumors. SIGNIFICANCE: T-cell metabolism plays a central role in T-cell fate yet is altered in cancer in ways that can suppress antitumor immunity. Here, we discuss challenges and opportunities to stimulate effector T-cell metabolism and improve cancer immunotherapy.
    MeSH term(s) Humans ; Immunotherapy, Adoptive ; Neoplasms/therapy ; T-Lymphocytes/metabolism ; Tumor Microenvironment
    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-20-0569
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Cancer cell metabolism and antitumour immunity.

    De Martino, Mara / Rathmell, Jeffrey C / Galluzzi, Lorenzo / Vanpouille-Box, Claire

    Nature reviews. Immunology

    2024  

    Abstract: Accumulating evidence suggests that metabolic rewiring in malignant cells supports tumour progression not only by providing cancer cells with increased proliferative potential and an improved ability to adapt to adverse microenvironmental conditions but ... ...

    Abstract Accumulating evidence suggests that metabolic rewiring in malignant cells supports tumour progression not only by providing cancer cells with increased proliferative potential and an improved ability to adapt to adverse microenvironmental conditions but also by favouring the evasion of natural and therapy-driven antitumour immune responses. Here, we review cancer cell-intrinsic and cancer cell-extrinsic mechanisms through which alterations of metabolism in malignant cells interfere with innate and adaptive immune functions in support of accelerated disease progression. Further, we discuss the potential of targeting such alterations to enhance anticancer immunity for therapeutic purposes.
    Language English
    Publishing date 2024-04-22
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-024-01026-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Microenvironmental influences on T cell immunity in cancer and inflammation.

    Heintzman, Darren R / Fisher, Emilie L / Rathmell, Jeffrey C

    Cellular & molecular immunology

    2022  Volume 19, Issue 3, Page(s) 316–326

    Abstract: T cell metabolism is dynamic and highly regulated. While the intrinsic metabolic programs of T cell subsets are integral to their distinct differentiation and functional patterns, the ability of cells to acquire nutrients and cope with hostile ... ...

    Abstract T cell metabolism is dynamic and highly regulated. While the intrinsic metabolic programs of T cell subsets are integral to their distinct differentiation and functional patterns, the ability of cells to acquire nutrients and cope with hostile microenvironments can limit these pathways. T cells must function in a wide variety of tissue settings, and how T cells interpret these signals to maintain an appropriate metabolic program for their demands or if metabolic mechanisms of immune suppression restrain immunity is an area of growing importance. Both in inflamed and cancer tissues, a wide range of changes in physical conditions and nutrient availability are now acknowledged to shape immunity. These include fever and increased temperatures, depletion of critical micro and macro-nutrients, and accumulation of inhibitory waste products. Here we review several of these factors and how the tissue microenvironment both shapes and constrains immunity.
    MeSH term(s) Humans ; Inflammation ; Neoplasms ; T-Lymphocyte Subsets ; Tumor Microenvironment
    Language English
    Publishing date 2022-01-17
    Publishing country China
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/s41423-021-00833-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Mitochondrial Homeostasis in AML and Gasping for Response in Resistance to BCL2 Blockade.

    Savona, Michael R / Rathmell, Jeffrey C

    Cancer discovery

    2019  Volume 9, Issue 7, Page(s) 831–833

    Abstract: Understanding resistance to BCL2 inhibition is a critical scientific and clinical challenge. In this issue ... ...

    Abstract Understanding resistance to BCL2 inhibition is a critical scientific and clinical challenge. In this issue of
    MeSH term(s) Bridged Bicyclo Compounds, Heterocyclic ; Homeostasis ; Humans ; Leukemia, Myeloid, Acute ; Proto-Oncogene Proteins c-bcl-2 ; Sulfonamides
    Chemical Substances Bridged Bicyclo Compounds, Heterocyclic ; Proto-Oncogene Proteins c-bcl-2 ; Sulfonamides ; venetoclax (N54AIC43PW)
    Language English
    Publishing date 2019-07-03
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-19-0510
    Database MEDical Literature Analysis and Retrieval System OnLINE

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