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  1. Article ; Online: TREM2 function in glioblastoma immune microenvironment: can we distinguish reality from illusion?

    Ghosh, Sourav / Rothlin, Carla V

    Neuro-oncology

    2024  

    Language English
    Publishing date 2024-01-30
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 2028601-6
    ISSN 1523-5866 ; 1522-8517
    ISSN (online) 1523-5866
    ISSN 1522-8517
    DOI 10.1093/neuonc/noae019
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    Zs.A 5307: Show issues Location:
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  2. Article ; Online: When aging gets on the way of disposal: Senescent cell suppression of efferocytosis.

    Rothlin, Carla V / Ghosh, Sourav

    The Journal of cell biology

    2023  Volume 222, Issue 2

    Abstract: Chronic senescence can trigger pathological inflammation. In this issue, Schloesser et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202207097) demonstrate that senescent cells employ "don't eat me" signals that inhibit the ability of macrophages ... ...

    Abstract Chronic senescence can trigger pathological inflammation. In this issue, Schloesser et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202207097) demonstrate that senescent cells employ "don't eat me" signals that inhibit the ability of macrophages to engulf them and additionally prevent macrophages from removing neighboring corpses, revealing a new mechanism by which senescence may contribute to triggering inflammation.
    MeSH term(s) Humans ; Aging ; Cellular Senescence ; Inflammation ; Macrophages ; Phagocytosis
    Language English
    Publishing date 2023-01-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202212023
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  3. Article ; Online: Management of cell death in parasitic infections.

    Bosurgi, Lidia / Rothlin, Carla V

    Seminars in immunopathology

    2021  Volume 43, Issue 4, Page(s) 481–492

    Abstract: For a long time, host cell death during parasitic infection has been considered a reflection of tissue damage, and often associated with disease pathogenesis. However, during their evolution, protozoan and helminth parasites have developed strategies to ... ...

    Abstract For a long time, host cell death during parasitic infection has been considered a reflection of tissue damage, and often associated with disease pathogenesis. However, during their evolution, protozoan and helminth parasites have developed strategies to interfere with cell death so as to spread and survive in the infected host, thereby ascribing a more intriguing role to infection-associated cell death. In this review, we examine the mechanisms used by intracellular and extracellular parasites to respectively inhibit or trigger programmed cell death. We further dissect the role of the prototypical "eat-me signal" phosphatidylserine (PtdSer) which, by being exposed on the cell surface of damaged host cells as well as on some viable parasites via a process of apoptotic mimicry, leads to their recognition and up-take by the neighboring phagocytes. Although barely dissected so far, the engagement of different PtdSer receptors on macrophages, by shaping the host immune response, affects the overall infection outcome in models of both protozoan and helminth infections. In this scenario, further understanding of the molecular and cellular regulation of the PtdSer exposing cell-macrophage interaction might allow the identification of new therapeutic targets for the management of parasitic infection.
    MeSH term(s) Animals ; Apoptosis ; Humans ; Macrophages ; Parasites ; Parasitic Diseases ; Phosphatidylserines
    Chemical Substances Phosphatidylserines
    Language English
    Publishing date 2021-07-19
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-021-00875-8
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  4. Article ; Online: Cracking the Cell Death Code.

    Rothlin, Carla V / Ghosh, Sourav

    Cold Spring Harbor perspectives in biology

    2020  Volume 12, Issue 5

    Abstract: Cell death is an invariant feature throughout our life span, starting with extensive scheduled cell death during morphogenesis and continuing with death under homeostasis in adult tissues. Additionally, cells become victims of accidental, unscheduled ... ...

    Abstract Cell death is an invariant feature throughout our life span, starting with extensive scheduled cell death during morphogenesis and continuing with death under homeostasis in adult tissues. Additionally, cells become victims of accidental, unscheduled death following injury and infection. Cell death in each of these occasions triggers specific and specialized responses in the living cells that surround them or are attracted to the dying/dead cells. These responses sculpt tissues during morphogenesis, replenish lost cells in homeostasis to maintain tissue/system function, and repair damaged tissues after injury. Wherein lies the information that sets in motion the cascade of effector responses culminating in remodeling, renewal, or repair? Here, we attempt to provide a framework for thinking about cell death in terms of the specific effector responses that accompanies various modalities of cell death. We also propose an integrated threefold "cell death code" consisting of information intrinsic to the dying/dead cell, the surroundings of the dying cell, and the identity of the responder.
    MeSH term(s) Animals ; Apoptosis ; Cell Death/physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cell Proliferation ; Cytosol/metabolism ; Embryonic Development ; Homeostasis ; Humans ; Macrophages/metabolism ; Models, Biological ; Morphogenesis ; Neurons/metabolism
    Language English
    Publishing date 2020-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1943-0264
    ISSN (online) 1943-0264
    DOI 10.1101/cshperspect.a036343
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  5. Article ; Online: Editorial overview: Innate immunity, from host defense and beyond.

    Rothlin, Carla V / Rathinam, Vijay A / Ghosh, Sourav

    Current opinion in immunology

    2021  Volume 68, Page(s) iii–v

    MeSH term(s) Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/immunology
    Language English
    Publishing date 2021-03-02
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2021.02.005
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    Zs.A 2773: Show issues Location:
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    Zs.MG 13: Show issues

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  6. Article ; Online: Lifting the innate immune barriers to antitumor immunity.

    Rothlin, Carla V / Ghosh, Sourav

    Journal for immunotherapy of cancer

    2020  Volume 8, Issue 1

    Abstract: The immune system evolved for adequate surveillance and killing of pathogens while minimizing host damage, such as due to chronic or exaggerated inflammation and autoimmunity. This is achieved by negative regulators and checkpoints that limit the ... ...

    Abstract The immune system evolved for adequate surveillance and killing of pathogens while minimizing host damage, such as due to chronic or exaggerated inflammation and autoimmunity. This is achieved by negative regulators and checkpoints that limit the magnitude and time course of the immune response. Tumor cells often escape immune surveillance and killing. Therefore, disrupting the brakes built into the immune system should effectively boost the anticancer immune response. The success of anti-CTLA4, anti-PD-1 and anti-PD-L1 have firmly established this proof of concept. Since the response rate of anti-CTLA4, anti-PD-1 and anti-PD-L1 is still limited, there is an intense effort for the identification of new targets and development of approaches that can expand the benefits of immunotherapy to a larger patient pool. Additional T cell checkpoints are obvious targets; however, here we focus on the unusual suspects-cells that function to initiate and guide T cell activity. Innate immunity is both an obligate prerequisite for the initiation of adaptive immune responses and a requirement for the recruitment of activated T cells to the site of action. We discuss some of the molecules present in innate immune cells, including natural killer cells, dendritic cells, macrophages, myeloid-derived suppressor cells, endothelial cells and stromal cells, that can activate or enhance innate immune cell functions, and more importantly, the inhibitors or checkpoints present in these cells that restrain their functions. Boosting innate immunity, either by enhancing activator functions or, preferably, by blocking the inhibitors, may represent a new anticancer treatment modality or at least function as adjuvants to T cell checkpoint inhibitors.
    MeSH term(s) Humans ; Immunity, Innate/immunology ; Immunotherapy/methods ; Neoplasms/immunology
    Language English
    Publishing date 2020-03-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2719863-7
    ISSN 2051-1426 ; 2051-1426
    ISSN (online) 2051-1426
    ISSN 2051-1426
    DOI 10.1136/jitc-2020-000695
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  7. Article ; Online: Serous macrophages pack Bhlhe40 for a randonnée.

    Rothlin, Carla V / Ghosh, Sourav

    Nature immunology

    2019  Volume 20, Issue 6, Page(s) 670–671

    MeSH term(s) Basic Helix-Loop-Helix Transcription Factors ; Cell Proliferation ; Homeodomain Proteins ; Homeostasis ; Macrophages
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Homeodomain Proteins
    Language English
    Publishing date 2019-05-06
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-019-0373-6
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    Zs.A 5294: Show issues Location:
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    Zs.MG 42: Show issues

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  8. Article ; Online: Determining the effector response to cell death.

    Rothlin, Carla V / Hille, Thomas D / Ghosh, Sourav

    Nature reviews. Immunology

    2020  Volume 21, Issue 5, Page(s) 292–304

    Abstract: Cell death occurs when a pathogen invades a host organism or the organism is subjected to sterile injury. Thus, cell death is often closely associated with the induction of an immune response. Furthermore, cell death can occur as a consequence of the ... ...

    Abstract Cell death occurs when a pathogen invades a host organism or the organism is subjected to sterile injury. Thus, cell death is often closely associated with the induction of an immune response. Furthermore, cell death can occur as a consequence of the immune response and precedes the tissue renewal and repair responses that are initiated by innate immune cells during resolution of an immune response. Beyond immunity, cell death is required for development, morphogenesis and homeostasis. How can such a ubiquitous event as cell death trigger such a wide range of context-specific effector responses? Dying cells are sensed by innate immune cells using specialized receptors and phagocytosed through a process termed efferocytosis. Here, we outline a general principle whereby signals within the dead cell as well as the environment are integrated by specific efferocytes to define the appropriate effector response.
    MeSH term(s) Animals ; Cell Death/immunology ; Cellular Microenvironment/immunology ; Cytokines/immunology ; Homeostasis/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Mathematical Concepts ; Models, Immunological ; Phagocytes/classification ; Phagocytes/immunology ; Phagocytosis/immunology ; Signal Transduction/immunology
    Chemical Substances Cytokines
    Language English
    Publishing date 2020-11-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-020-00456-0
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    Zs.A 5565: Show issues Location:
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    Zs.MG 34: Show issues

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  9. Article ; Online: Cell death in development, maintenance, and diseases of the nervous system.

    Mercau, Maria E / Patwa, Siraj / Bhat, Krishna P L / Ghosh, Sourav / Rothlin, Carla V

    Seminars in immunopathology

    2022  Volume 44, Issue 5, Page(s) 725–738

    Abstract: Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis-especially in context of adult neurogenesis. ... ...

    Abstract Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis-especially in context of adult neurogenesis. Finally, cell death is commonplace in acute brain injuries, chronic neurodegenerative diseases, and in some central nervous system tumors such as glioblastoma. Recent studies are enumerating the various molecular modalities involved in the execution of cells. Intimately linked with cell death are mechanisms of disposal that remove the dead cell and bring about a tissue-level response. Heretofore, the association between these methods of dying and physiological or pathological responses has remained nebulous. It is envisioned that careful cartography of death and disposal may reveal novel understandings of disease states and chart new therapeutic strategies in the near future.
    MeSH term(s) Adult ; Cell Death ; Homeostasis ; Humans ; Nervous System ; Neurogenesis/physiology ; Neurons
    Language English
    Publishing date 2022-05-04
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-022-00938-4
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  10. Article ; Online: Bringing on the itch.

    Waizman, Daniel A / Ghosh, Sourav / Rothlin, Carla V

    eLife

    2019  Volume 8

    Abstract: Neutrophils are the first immune cells that enter the skin and cause itch in atopic dermatitis. ...

    Abstract Neutrophils are the first immune cells that enter the skin and cause itch in atopic dermatitis.
    MeSH term(s) Dermatitis, Atopic ; Humans ; Pruritus ; Skin
    Language English
    Publishing date 2019-11-29
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.52931
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