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  1. Article ; Online: The ins and outs of microglial cells in brain health and disease.

    Pallarés-Moratalla, Carla / Bergers, Gabriele

    Frontiers in immunology

    2024  Volume 15, Page(s) 1305087

    Abstract: Microglia are the brain's resident macrophages that play pivotal roles in immune surveillance and maintaining homeostasis of the Central Nervous System (CNS). Microglia are functionally implicated in various cerebrovascular diseases, including stroke, ... ...

    Abstract Microglia are the brain's resident macrophages that play pivotal roles in immune surveillance and maintaining homeostasis of the Central Nervous System (CNS). Microglia are functionally implicated in various cerebrovascular diseases, including stroke, aneurysm, and tumorigenesis as they regulate neuroinflammatory responses and tissue repair processes. Here, we review the manifold functions of microglia in the brain under physiological and pathological conditions, primarily focusing on the implication of microglia in glioma propagation and progression. We further review the current status of therapies targeting microglial cells, including their re-education, depletion, and re-population approaches as therapeutic options to improve patient outcomes for various neurological and neuroinflammatory disorders, including cancer.
    MeSH term(s) Humans ; Microglia/immunology ; Brain/immunology ; Brain/pathology ; Animals ; Neuroinflammatory Diseases/immunology ; Neuroinflammatory Diseases/pathology ; Brain Diseases/immunology ; Brain Diseases/pathology ; Glioma/immunology ; Glioma/pathology ; Glioma/therapy
    Language English
    Publishing date 2024-04-11
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1305087
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: R-2-HG assists IDH1-mutant solid tumors by promoting angiogenesis.

    Bögürcü-Seidel, Nuray / Bergers, Gabriele

    Cell research

    2022  Volume 32, Issue 9, Page(s) 795–796

    MeSH term(s) Glioma/pathology ; Humans ; Isocitrate Dehydrogenase/genetics ; Mutation/genetics
    Chemical Substances Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.)
    Language English
    Publishing date 2022-07-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-022-00708-9
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5283: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  3. Article ; Online: High endothelial venules in cancer: Regulation, function, and therapeutic implication.

    Vella, Gerlanda / Hua, Yichao / Bergers, Gabriele

    Cancer cell

    2023  Volume 41, Issue 3, Page(s) 527–545

    Abstract: The lack of sufficient intratumoral ... ...

    Abstract The lack of sufficient intratumoral CD8
    MeSH term(s) Humans ; Mice ; Animals ; Venules/pathology ; Neoplasms/therapy ; Neoplasms/pathology ; Lymph Nodes ; T-Lymphocytes ; Lymphocytes ; Tumor Microenvironment
    Language English
    Publishing date 2023-02-23
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2023.02.002
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5650: Show issues Location:
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    Zs.MG 104: Show issues

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  4. Article ; Online: The metabolism of cancer cells during metastasis.

    Bergers, Gabriele / Fendt, Sarah-Maria

    Nature reviews. Cancer

    2021  Volume 21, Issue 3, Page(s) 162–180

    Abstract: Metastasis formation is the major cause of death in most patients with cancer. Despite extensive research, targeting metastatic seeding and colonization is still an unresolved challenge. Only recently, attention has been drawn to the fact that ... ...

    Abstract Metastasis formation is the major cause of death in most patients with cancer. Despite extensive research, targeting metastatic seeding and colonization is still an unresolved challenge. Only recently, attention has been drawn to the fact that metastasizing cancer cells selectively and dynamically adapt their metabolism at every step during the metastatic cascade. Moreover, many metastases display different metabolic traits compared with the tumours from which they originate, enabling survival and growth in the new environment. Consequently, the stage-dependent metabolic traits may provide therapeutic windows for preventing or reducing metastasis, and targeting the new metabolic traits arising in established metastases may allow their eradication.
    MeSH term(s) Acetates/metabolism ; Adenosine Triphosphate/biosynthesis ; Animals ; Cell Plasticity ; Fatty Acids/metabolism ; Glutamine/metabolism ; Humans ; Lactic Acid/metabolism ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Cells, Circulating/metabolism ; Pyruvic Acid/metabolism
    Chemical Substances Acetates ; Fatty Acids ; Glutamine (0RH81L854J) ; Lactic Acid (33X04XA5AT) ; Pyruvic Acid (8558G7RUTR) ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2021-01-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-020-00320-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5563: Show issues Location:
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    Zs.MG 24: Show issues

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  5. Article ; Online: High Endothelial Venules: A Vascular Perspective on Tertiary Lymphoid Structures in Cancer.

    Vella, Gerlanda / Guelfi, Sophie / Bergers, Gabriele

    Frontiers in immunology

    2021  Volume 12, Page(s) 736670

    Abstract: High endothelial venules (HEVs) are specialized postcapillary venules composed of cuboidal blood endothelial cells that express high levels of sulfated sialomucins to bind L-Selectin/CD62L on lymphocytes, thereby facilitating their transmigration from ... ...

    Abstract High endothelial venules (HEVs) are specialized postcapillary venules composed of cuboidal blood endothelial cells that express high levels of sulfated sialomucins to bind L-Selectin/CD62L on lymphocytes, thereby facilitating their transmigration from the blood into the lymph nodes (LN) and other secondary lymphoid organs (SLO). HEVs have also been identified in human and murine tumors in predominantly CD3
    MeSH term(s) Animals ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Immunotherapy ; L-Selectin/metabolism ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Neoplasms/blood supply ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Sialomucins/metabolism ; Signal Transduction ; Tertiary Lymphoid Structures/immunology ; Tertiary Lymphoid Structures/metabolism ; Tertiary Lymphoid Structures/pathology ; Transendothelial and Transepithelial Migration ; Tumor Microenvironment ; Venules/immunology ; Venules/metabolism ; Venules/pathology
    Chemical Substances SELL protein, human ; Sialomucins ; L-Selectin (126880-86-2)
    Language English
    Publishing date 2021-08-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.736670
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Tumors vs. Chronic Wounds: An Immune Cell's Perspective.

    Hua, Yichao / Bergers, Gabriele

    Frontiers in immunology

    2019  Volume 10, Page(s) 2178

    Abstract: The wound repair program is tightly regulated and coordinated among different cell constituents including epithelial cells, fibroblasts, immune cells and endothelial cells following consecutive steps to ensure timely, and proper wound closure. ... ...

    Abstract The wound repair program is tightly regulated and coordinated among different cell constituents including epithelial cells, fibroblasts, immune cells and endothelial cells following consecutive steps to ensure timely, and proper wound closure. Specifically, innate and adaptive immune cells are pivotal participants that also closely interact with the vasculature. Tumors are portrayed as wounds that do not heal because they undergo continuous stromal remodeling and vascular growth with immunosuppressive features to ensure tumor propagation; a stage that is reminiscent of the proliferative resolution phase in wound repair. There is increasing evidence from mouse model systems and clinical trials that targeting both the immune and vascular compartments is an attractive therapeutic approach to reawaken the inflammatory status in the "tumor wound" with the final goal to abrogate tumor cells and invigorate tissue homeostasis. In this review, we compare the implication of immune cells and the vasculature in chronic wounds and tumor wounds to underscore the conceptual idea of transitioning tumors into an inflammatory wound-like state with antiangiogenic immunotherapies to improve beneficial effects in cancer patients.
    MeSH term(s) Animals ; Endothelial Cells/immunology ; Endothelial Cells/pathology ; Humans ; Immunotherapy ; Inflammation/immunology ; Inflammation/pathology ; Inflammation/therapy ; Mice ; Neoplasms/blood supply ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Neovascularization, Pathologic/immunology ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/therapy ; Wound Healing/immunology ; Wounds and Injuries/immunology ; Wounds and Injuries/pathology ; Wounds and Injuries/therapy
    Language English
    Publishing date 2019-09-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.02178
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  7. Article ; Online: Where Have All the T Cells Gone?

    Vella, Gerlanda / Bergers, Gabriele

    Immunity

    2018  Volume 49, Issue 4, Page(s) 592–594

    Abstract: Glioblastoma are highly immunosuppressive brain tumors that are known for their T cell paucity. In a recent issue of Nature Medicine, Chongsathidkiet et al. (2018) discovered a brain-specific mechanism of tumors to escape immunosurveillance by trapping T  ...

    Abstract Glioblastoma are highly immunosuppressive brain tumors that are known for their T cell paucity. In a recent issue of Nature Medicine, Chongsathidkiet et al. (2018) discovered a brain-specific mechanism of tumors to escape immunosurveillance by trapping T cells in the bone marrow through the loss of sphingosine-1-phosphate (S1P) receptor on the T cell surface.
    MeSH term(s) Adult ; Bone Marrow ; Brain Neoplasms ; Glioblastoma ; Humans ; Lysophospholipids ; Receptors, Lysosphingolipid ; Sphingosine ; T-Lymphocytes
    Chemical Substances Lysophospholipids ; Receptors, Lysosphingolipid ; Sphingosine (NGZ37HRE42)
    Language English
    Publishing date 2018-10-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2018.10.006
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4227: Show issues Location:
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    Zs.MG 69: Show issues

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  8. Article ; Online: Regulation of Blood and Lymphatic Vessels by Immune Cells in Tumors and Metastasis.

    Mazzone, Massimiliano / Bergers, Gabriele

    Annual review of physiology

    2018  Volume 81, Page(s) 535–560

    Abstract: Research over the last decades has provided strong evidence for the pivotal role of the tumor-associated blood and lymphatic vasculature in supporting immunoevasion and in subverting T cell-mediated immunosurveillance. Conversely, tumor blood and ... ...

    Abstract Research over the last decades has provided strong evidence for the pivotal role of the tumor-associated blood and lymphatic vasculature in supporting immunoevasion and in subverting T cell-mediated immunosurveillance. Conversely, tumor blood and lymphatic vessel growth is in part regulated by the immune system, with infiltrating innate as well as adaptive immune cells providing both immunosuppressive and various angiogenic signals. Thus, tumor angiogenesis and escape of immunosurveillance are two cancer hallmarks that are tightly linked and interregulated by cell constituents from compartments secreting both chemokines and cytokines. In this review, we discuss the implication and regulation of innate and adaptive immune cells in regulating blood and lymphatic angiogenesis in tumor progression and metastases. Moreover, we also highlight novel therapeutic approaches that target the tumor vasculature as well as the immune compartment to sustain and improve therapeutic efficacy in cancer.
    MeSH term(s) Angiogenesis Inhibitors/therapeutic use ; Animals ; Blood Vessels ; Cytokines/physiology ; Humans ; Immune System/metabolism ; Immunotherapy ; Lymphatic Vessels ; Neoplasms/physiopathology ; Neovascularization, Pathologic
    Chemical Substances Angiogenesis Inhibitors ; Cytokines
    Language English
    Publishing date 2018-11-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 207933-1
    ISSN 1545-1585 ; 0066-4278
    ISSN (online) 1545-1585
    ISSN 0066-4278
    DOI 10.1146/annurev-physiol-020518-114721
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    Uc I Zs.226: Show issues Location:
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  9. Article ; Online: Therapeutic induction of high endothelial venules (HEVs) to enhance T-cell infiltration in tumors.

    Allen, Elizabeth / Missiaen, Rindert / Bergers, Gabriele

    Oncotarget

    2017  Volume 8, Issue 59, Page(s) 99207–99208

    Language English
    Publishing date 2017-11-21
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.22276
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  10. Article ; Online: An autophagy program that promotes T cell egress from the lymph node controls responses to immune checkpoint blockade.

    Houbaert, Diede / Nikolakopoulos, Apostolos Panagiotis / Jacobs, Kathryn A / Meçe, Odeta / Roels, Jana / Shankar, Gautam / Agrawal, Madhur / More, Sanket / Ganne, Maarten / Rillaerts, Kristine / Boon, Louis / Swoboda, Magdalena / Nobis, Max / Mourao, Larissa / Bosisio, Francesca / Vandamme, Niels / Bergers, Gabriele / Scheele, Colinda L G J / Agostinis, Patrizia

    Cell reports

    2024  Volume 43, Issue 4, Page(s) 114020

    Abstract: Lymphatic endothelial cells (LECs) of the lymph node (LN) parenchyma orchestrate leukocyte trafficking and peripheral T cell dynamics. T cell responses to immunotherapy largely rely on peripheral T cell recruitment in tumors. Yet, a systematic and ... ...

    Abstract Lymphatic endothelial cells (LECs) of the lymph node (LN) parenchyma orchestrate leukocyte trafficking and peripheral T cell dynamics. T cell responses to immunotherapy largely rely on peripheral T cell recruitment in tumors. Yet, a systematic and molecular understanding of how LECs within the LNs control T cell dynamics under steady-state and tumor-bearing conditions is lacking. Intravital imaging combined with immune phenotyping shows that LEC-specific deletion of the essential autophagy gene Atg5 alters intranodal positioning of lymphocytes and accrues their persistence in the LNs by increasing the availability of the main egress signal sphingosine-1-phosphate. Single-cell RNA sequencing of tumor-draining LNs shows that loss of ATG5 remodels niche-specific LEC phenotypes involved in molecular pathways regulating lymphocyte trafficking and LEC-T cell interactions. Functionally, loss of LEC autophagy prevents recruitment of tumor-infiltrating T and natural killer cells and abrogates response to immunotherapy. Thus, an LEC-autophagy program boosts immune-checkpoint responses by guiding systemic T cell dynamics.
    MeSH term(s) Autophagy/drug effects ; Animals ; Lymph Nodes/immunology ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Mice ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Mice, Inbred C57BL ; Autophagy-Related Protein 5/metabolism ; Autophagy-Related Protein 5/genetics ; Endothelial Cells/metabolism ; Sphingosine/analogs & derivatives ; Sphingosine/pharmacology ; Sphingosine/metabolism ; Humans ; Lysophospholipids/metabolism ; Immunotherapy/methods ; Cell Movement
    Chemical Substances Immune Checkpoint Inhibitors ; Autophagy-Related Protein 5 ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42) ; Lysophospholipids ; Atg5 protein, mouse
    Language English
    Publishing date 2024-03-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.114020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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