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  1. Article ; Online: MIF-Dependent Control of Tumor Immunity.

    Noe, Jordan T / Mitchell, Robert A

    Frontiers in immunology

    2020  Volume 11, Page(s) 609948

    Abstract: Initially identified as a T lymphocyte-elicited inhibitor of macrophage motility, macrophage migration inhibitory factor (MIF) has since been found to be expressed by nearly every immune cell type examined and overexpressed in most solid and hematogenous ...

    Abstract Initially identified as a T lymphocyte-elicited inhibitor of macrophage motility, macrophage migration inhibitory factor (MIF) has since been found to be expressed by nearly every immune cell type examined and overexpressed in most solid and hematogenous malignant cancers. It is localized to both extracellular and intracellular compartments and physically interacts with more than a dozen different cell surface and intracellular proteins. Although classically associated with and characterized as a mediator of pro-inflammatory innate immune responses, more recent studies demonstrate that, in malignant disease settings, MIF contributes to anti-inflammatory, immune evasive, and immune tolerant phenotypes in both innate and adaptive immune cell types. This review will summarize the studies describing MIF in tumor-specific innate and adaptive immune responses and attempt to reconcile these various pleiotropic functions in normal physiology.
    MeSH term(s) Adaptive Immunity ; Animals ; Cell Communication ; Humans ; Immunity, Innate ; Immunotherapy ; Intramolecular Oxidoreductases/metabolism ; Macrophage Migration-Inhibitory Factors/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction ; Tumor Escape ; Tumor Microenvironment
    Chemical Substances Macrophage Migration-Inhibitory Factors ; Intramolecular Oxidoreductases (EC 5.3.-) ; MIF protein, human (EC 5.3.2.1)
    Language English
    Publishing date 2020-11-25
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.609948
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Tricarboxylic acid cycle metabolites in the control of macrophage activation and effector phenotypes.

    Noe, Jordan T / Mitchell, Robert A

    Journal of leukocyte biology

    2019  Volume 106, Issue 2, Page(s) 359–367

    Abstract: The tricarboxylic acid (TCA) cycle is a mitochondrial metabolic hub that coordinates the metabolism of carbohydrates, proteins, and fats into carbon dioxide and ATP. At specific points in the cycle, the diversion, import, or export of TCA metabolites ... ...

    Abstract The tricarboxylic acid (TCA) cycle is a mitochondrial metabolic hub that coordinates the metabolism of carbohydrates, proteins, and fats into carbon dioxide and ATP. At specific points in the cycle, the diversion, import, or export of TCA metabolites allows for the dynamic regulation of a variety of tissue and/or cell-specific phenotypic processes. Recent studies have identified that a number of TCA metabolites are important in controlling monocyte/macrophage phenotypes and effector functions while specific macrophage activation or polarization states functionally determine the relative utilization of each. This review focuses on the metabolic reprogramming of the TCA cycle in macrophages and how individual metabolites play a variety of context-specific roles in determining physiologic and pathologic macrophage activation and homeostatic functions. We discuss the implications of these findings and address unanswered questions regarding the role of the TCA cycle in guiding macrophage-dependent immune responses.
    MeSH term(s) Animals ; Biomarkers ; Cellular Reprogramming ; Citric Acid Cycle ; Energy Metabolism ; Humans ; Macrophage Activation/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Mitochondria/metabolism ; Phenotype
    Chemical Substances Biomarkers
    Language English
    Publishing date 2019-02-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.3RU1218-496R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A Tumor-admixture Model to Interrogate Immune Cell-dependent Tumorigenesis.

    Noe, Jordan T / Ding, Chuanlin / Geller, Anne E / Rendon, Beatriz E / Yan, Jun / Mitchell, Robert A

    Bio-protocol

    2023  Volume 13, Issue 5

    Abstract: A rigorous determination of effector contributions of tumor-infiltrating immune cells is critical for identifying targetable molecular mechanisms for the development of novel cancer immunotherapies. A tumor/immune cell-admixture model is an advantageous ... ...

    Abstract A rigorous determination of effector contributions of tumor-infiltrating immune cells is critical for identifying targetable molecular mechanisms for the development of novel cancer immunotherapies. A tumor/immune cell-admixture model is an advantageous strategy to study tumor immunology as the fundamental methodology is relatively straightforward, while also being adaptable to scale to address increasingly complex research queries. Ultimately, this method can provide robust experimental information to complement more traditional murine models of tumor immunology. Here, we describe a tumor/macrophage-admixture model using bone marrow-derived macrophages to investigate macrophage-dependent tumorigenesis. Additionally, we provide commentary on potential branch points for optimization with other immune cells, experimental techniques, and cancer types.
    Language English
    Publishing date 2023-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4630
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Lactate supports a metabolic-epigenetic link in macrophage polarization.

    Noe, Jordan T / Rendon, Beatriz E / Geller, Anne E / Conroy, Lindsey R / Morrissey, Samantha M / Young, Lyndsay E A / Bruntz, Ronald C / Kim, Eun J / Wise-Mitchell, Ashley / Barbosa de Souza Rizzo, Mariana / Relich, Eric R / Baby, Becca V / Johnson, Lance A / Affronti, Hayley C / McMasters, Kelly M / Clem, Brian F / Gentry, Matthew S / Yan, Jun / Wellen, Kathryn E /
    Sun, Ramon C / Mitchell, Robert A

    Science advances

    2021  Volume 7, Issue 46, Page(s) eabi8602

    Abstract: Lactate accumulation is a hallmark of solid cancers and is linked to the immune suppressive phenotypes of tumor-infiltrating immune cells. We report herein that interleukin-4 (IL-4)–induced M0 → M2 macrophage polarization is accompanied by ... ...

    Abstract Lactate accumulation is a hallmark of solid cancers and is linked to the immune suppressive phenotypes of tumor-infiltrating immune cells. We report herein that interleukin-4 (IL-4)–induced M0 → M2 macrophage polarization is accompanied by interchangeable glucose- or lactate-dependent tricarboxylic acid (TCA) cycle metabolism that directly drives histone acetylation, M2 gene transcription, and functional immune suppression. Lactate-dependent M0 → M2 polarization requires both mitochondrial pyruvate uptake and adenosine triphosphate–citrate lyase (ACLY) enzymatic activity. Notably, exogenous acetate rescues defective M2 polarization and histone acetylation following mitochondrial pyruvate carrier 1 (MPC1) inhibition or ACLY deficiency. Lastly, M2 macrophage–dependent tumor progression is impaired by conditional macrophage ACLY deficiency, further supporting a dominant role for glucose/lactate mitochondrial metabolism and histone acetylation in driving immune evasion. This work adds to our understanding of how mitochondrial metabolism affects macrophage functional phenotypes and identifies a unique tumor microenvironment (TME)–driven metabolic-epigenetic link in M2 macrophages.
    Language English
    Publishing date 2021-11-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abi8602
    Database MEDical Literature Analysis and Retrieval System OnLINE

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