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  1. Article ; Online: Dietary long-chain fatty acid metabolism boosts antitumor immune response.

    Wang, Jiaming / Cao, Xuetao

    Cancer communications (London, England)

    2024  

    Language English
    Publishing date 2024-04-12
    Publishing country United States
    Document type Journal Article
    ISSN 2523-3548
    ISSN (online) 2523-3548
    DOI 10.1002/cac2.12543
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The tumor niche can reprogram long-lived protumorigenic neutrophils.

    Wang, Jiaming / Cao, Xuetao

    Trends in immunology

    2024  Volume 45, Issue 3, Page(s) 155–157

    Abstract: The heterogeneity and plasticity of neutrophils in tumor-host interactions and how tumor signals induce reprogramming of neutrophil subpopulations need further investigation. Ng et al. recently reported that a hypoxic-glycolytic niche in mouse tumors ... ...

    Abstract The heterogeneity and plasticity of neutrophils in tumor-host interactions and how tumor signals induce reprogramming of neutrophil subpopulations need further investigation. Ng et al. recently reported that a hypoxic-glycolytic niche in mouse tumors could reprogram mature and immature neutrophils into a long-lived and terminally-differentiated subset, which promoted angiogenesis and tumor growth.
    MeSH term(s) Mice ; Animals ; Neutrophils/pathology ; Neoplasms/pathology
    Language English
    Publishing date 2024-02-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2024.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: ISG15 secretion exacerbates inflammation in SARS-CoV-2 infection.

    Cao, Xuetao

    Nature immunology

    2021  Volume 22, Issue 11, Page(s) 1360–1362

    MeSH term(s) COVID-19 ; Cytokines ; Humans ; Inflammation ; SARS-CoV-2 ; Ubiquitins
    Chemical Substances Cytokines ; Ubiquitins ; ISG15 protein, human (60267-61-0)
    Language English
    Publishing date 2021-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-021-01056-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: COVID-19: immunopathology and its implications for therapy.

    Cao, Xuetao

    Nature reviews. Immunology

    2020  Volume 20, Issue 5, Page(s) 269–270

    MeSH term(s) Antibodies, Monoclonal, Humanized/therapeutic use ; Antiviral Agents/therapeutic use ; COVID-19 ; Clinical Trials as Topic ; Coronavirus Infections/immunology ; Coronavirus Infections/pathology ; Coronavirus Infections/therapy ; Cytokines/immunology ; Humans ; Immunization, Passive ; Inflammation/pathology ; Mesenchymal Stem Cell Transplantation ; Pandemics ; Pneumonia, Viral/immunology ; Pneumonia, Viral/pathology ; Pneumonia, Viral/therapy
    Chemical Substances Antibodies, Monoclonal, Humanized ; Antiviral Agents ; Cytokines ; tocilizumab (I031V2H011)
    Keywords covid19
    Language English
    Publishing date 2020-04-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-020-0308-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Glucose metabolism of TAMs in tumor chemoresistance and metastasis.

    Liu, Juan / Cao, Xuetao

    Trends in cell biology

    2023  Volume 33, Issue 11, Page(s) 967–978

    Abstract: Tumor-associated macrophages (TAMs) are critical in promoting tumor progression and therapeutic resistance. In adapting to metabolic changes in the tumor microenvironment (TME), TAMs reprogram their metabolisms and acquire immunosuppressive and pro-tumor ...

    Abstract Tumor-associated macrophages (TAMs) are critical in promoting tumor progression and therapeutic resistance. In adapting to metabolic changes in the tumor microenvironment (TME), TAMs reprogram their metabolisms and acquire immunosuppressive and pro-tumor properties. Increased glucose metabolism in TAMs leads to the accumulation of a variety of oncometabolites that exhibit potent tumor-promoting capacity via regulating gene expression and signaling transduction. Glucose uptake also fuels O-GlcNAcylation and other post-translational modifications to promote pro-tumor polarization and function of TAMs. Glucose metabolism coordinates interactions between TAMs and various types of cells in the TME, creating a complex network that facilitates tumor progression. Targeting glucose metabolism represents a promising strategy to switch TAMs from pro-tumor toward anti-tumor function for cancer therapy.
    Language English
    Publishing date 2023-04-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2023.03.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Nutritional competition within tumor microenvironment dictates anti-tumor immunity.

    Fei, Yankang / Cao, Xuetao / Liu, Juan

    National science review

    2023  Volume 11, Issue 2, Page(s) nwad277

    Language English
    Publishing date 2023-11-01
    Publishing country China
    Document type Journal Article
    ZDB-ID 2745465-4
    ISSN 2053-714X ; 2053-714X
    ISSN (online) 2053-714X
    ISSN 2053-714X
    DOI 10.1093/nsr/nwad277
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: TLR9 triggers MyD88-independent anti-inflammatory signaling in lupus.

    Zhang, Shikun / Cao, Xuetao

    Trends in immunology

    2023  Volume 44, Issue 3, Page(s) 153–155

    Abstract: Activation of Toll-like receptor 7 (TLR7) can induce lupus in mice, whereas activation of TLR9 can prevent it, even though both receptors interact with myeloid differentiation primary response gene 88 (MyD88) for downstream signaling. How TLR9 triggers ... ...

    Abstract Activation of Toll-like receptor 7 (TLR7) can induce lupus in mice, whereas activation of TLR9 can prevent it, even though both receptors interact with myeloid differentiation primary response gene 88 (MyD88) for downstream signaling. How TLR9 triggers anti-inflammatory responses in autoimmunity is unclear. Leibler et al. recently reported that TLR9 initiates anti-inflammatory signaling and inhibits lupus pathogenesis in a MyD88-independent but ligand-dependent manner.
    MeSH term(s) Mice ; Animals ; Toll-Like Receptor 9/metabolism ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Mice, Knockout ; Signal Transduction ; Adaptor Proteins, Signal Transducing ; Toll-Like Receptor 7/genetics ; Toll-Like Receptor 7/metabolism ; Anti-Inflammatory Agents
    Chemical Substances Toll-Like Receptor 9 ; Myeloid Differentiation Factor 88 ; Adaptor Proteins, Signal Transducing ; Toll-Like Receptor 7 ; Anti-Inflammatory Agents ; Myd88 protein, mouse ; Tlr9 protein, mouse
    Language English
    Publishing date 2023-02-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2023.01.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: RBP-RNA interactions in the control of autoimmunity and autoinflammation.

    Liu, Juan / Cao, Xuetao

    Cell research

    2023  Volume 33, Issue 2, Page(s) 97–115

    Abstract: Autoimmunity and autoinflammation arise from aberrant immunological and inflammatory responses toward self-components, contributing to various autoimmune diseases and autoinflammatory diseases. RNA-binding proteins (RBPs) are essential for immune cell ... ...

    Abstract Autoimmunity and autoinflammation arise from aberrant immunological and inflammatory responses toward self-components, contributing to various autoimmune diseases and autoinflammatory diseases. RNA-binding proteins (RBPs) are essential for immune cell development and function, mainly via exerting post-transcriptional regulation of RNA metabolism and function. Functional dysregulation of RBPs and abnormities in RNA metabolism are closely associated with multiple autoimmune or autoinflammatory disorders. Distinct RBPs play critical roles in aberrant autoreactive inflammatory responses via orchestrating a complex regulatory network consisting of DNAs, RNAs and proteins within immune cells. In-depth characterizations of RBP-RNA interactomes during autoimmunity and autoinflammation will lead to a better understanding of autoimmune pathogenesis and facilitate the development of effective therapeutic strategies. In this review, we summarize and discuss the functions of RBP-RNA interactions in controlling aberrant autoimmune inflammation and their potential as biomarkers and therapeutic targets.
    MeSH term(s) Humans ; Autoimmunity ; RNA ; Autoimmune Diseases ; Gene Expression Regulation ; Inflammation
    Chemical Substances RNA (63231-63-0)
    Language English
    Publishing date 2023-01-05
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-022-00752-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: COVID-19

    Cao, Xuetao

    Nature Reviews Immunology

    immunopathology and its implications for therapy

    2020  Volume 20, Issue 5, Page(s) 269–270

    Keywords Immunology ; covid19
    Language English
    Publisher Springer Science and Business Media LLC
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-020-0308-3
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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