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  1. Article: Editorial: Immune modulation in tumor microenvironment: New perspectives for cancer immunotherapy.

    Deng, Zimu / Sun, Xuejun / Cao, Jian / Xiao, Qian

    Frontiers in cell and developmental biology

    2023  Volume 10, Page(s) 1103705

    Language English
    Publishing date 2023-01-04
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.1103705
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  2. Article: Activated STING in the thymus alters T cell development and selection leading to autoimmunity.

    Deng, Zimu / Law, Christopher S / Kurra, Santosh / Simchoni, Noa / Shum, Anthony K

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Classifying systemic inflammatory disorders as autoinflammatory or autoimmune provides insight into disease pathogenesis and whether treatment should target innate molecules and their signaling pathways or the adaptive immune response. COPA syndrome is a ...

    Abstract Classifying systemic inflammatory disorders as autoinflammatory or autoimmune provides insight into disease pathogenesis and whether treatment should target innate molecules and their signaling pathways or the adaptive immune response. COPA syndrome is a monogenic disorder of immune dysregulation that leads to interstitial lung disease and high-titer autoantibodies. Studies show constitutive activation of the innate immune molecule STING is centrally involved in disease. However, the mechanisms by which STING results in loss of T cell tolerance and autoimmunity in COPA syndrome or more common autoimmune diseases is not understood. Using
    Language English
    Publishing date 2024-02-19
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.17.580803
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Neutrophils restrain sepsis associated coagulopathy via extracellular vesicles carrying superoxide dismutase 2 in a murine model of lipopolysaccharide induced sepsis.

    Bao, Wenjie / Xing, Huayue / Cao, Shiwei / Long, Xin / Liu, Haifeng / Ma, Junwei / Guo, Fan / Deng, Zimu / Liu, Xiaolong

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 4583

    Abstract: Disseminated intravascular coagulation (DIC) is a complication of sepsis currently lacking effective therapeutic options. Excessive inflammatory responses are emerging triggers of coagulopathy during sepsis, but the interplay between the immune system ... ...

    Abstract Disseminated intravascular coagulation (DIC) is a complication of sepsis currently lacking effective therapeutic options. Excessive inflammatory responses are emerging triggers of coagulopathy during sepsis, but the interplay between the immune system and coagulation are not fully understood. Here we utilize a murine model of intraperitoneal lipopolysaccharide stimulation and show neutrophils in the circulation mitigate the occurrence of DIC, preventing subsequent septic death. We show circulating neutrophils release extracellular vesicles containing mitochondria, which contain superoxide dismutase 2 upon exposure to lipopolysaccharide. Extracellular superoxide dismutase 2 is necessary to induce neutrophils' antithrombotic function by preventing endothelial reactive oxygen species accumulation and alleviating endothelial dysfunction. Intervening endothelial reactive oxygen species accumulation by antioxidants significantly ameliorates disseminated intravascular coagulation improving survival in this murine model of lipopolysaccharide challenge. These findings reveal an interaction between neutrophils and vascular endothelium which critically regulate coagulation in a model of sepsis and may have potential implications for the management of disseminated intravascular coagulation.
    MeSH term(s) Animals ; Blood Coagulation Disorders ; Disease Models, Animal ; Disseminated Intravascular Coagulation/etiology ; Extracellular Vesicles ; Lipopolysaccharides/toxicity ; Mice ; Neutrophils ; Reactive Oxygen Species ; Sepsis/complications ; Superoxide Dismutase/metabolism
    Chemical Substances Lipopolysaccharides ; Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1) ; superoxide dismutase 2 (EC 1.15.1.1)
    Language English
    Publishing date 2022-08-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-32325-w
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  4. Article ; Online: CBX4 deletion promotes tumorigenesis under Kras

    Chen, Fangzhen / Hou, Wulei / Yu, Xiangtian / Wu, Jing / Li, Zhengda / Xu, Jietian / Deng, Zimu / Chen, Gaobin / Liu, Bo / Yin, Xiaoxing / Yu, Wei / Zhang, Lei / Xu, Guoliang / Ji, Hongbin / Liang, Chunmin / Wang, Zuoyun

    Signal transduction and targeted therapy

    2023  Volume 8, Issue 1, Page(s) 343

    Abstract: Chromobox protein homolog 4 (CBX4) is a component of the Polycomb group (PcG) multiprotein Polycomb repressive complexes 1 (PRC1), which is participated in several processes including growth, senescence, immunity, and tissue repair. CBX4 has been shown ... ...

    Abstract Chromobox protein homolog 4 (CBX4) is a component of the Polycomb group (PcG) multiprotein Polycomb repressive complexes 1 (PRC1), which is participated in several processes including growth, senescence, immunity, and tissue repair. CBX4 has been shown to have diverse, even opposite functions in different types of tissue and malignancy in previous studies. In this study, we found that CBX4 deletion promoted lung adenocarcinoma (LUAD) proliferation and progression in Kras
    MeSH term(s) Animals ; Humans ; Mice ; Adenocarcinoma of Lung/genetics ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic/genetics ; Chromosomal Instability ; Fibroblasts ; Genomic Instability/genetics ; Ligases/genetics ; Lung Neoplasms/genetics ; Polycomb Repressive Complex 1/genetics
    Chemical Substances Ligases (EC 6.-) ; Cbx4 protein, mouse (EC 6.3.2.-) ; Polycomb Repressive Complex 1 (EC 2.3.2.27)
    Language English
    Publishing date 2023-09-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-023-01623-0
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  5. Article ; Online: Reconstituted Thymus Organ Culture.

    Deng, Zimu / Liu, Haifeng / Rui, Jinxiu / Liu, Xiaolong

    Methods in molecular biology (Clifton, N.J.)

    2016  Volume 1323, Page(s) 151–158

    Abstract: Reconstituted thymus organ culture is based on fetal thymus organ culture (FTOC). Purified thymocyte populations, from genetically modified mice or even from other species, are cultured in vitro with thymic lobes depleted of their endogenous thymocytes ( ... ...

    Abstract Reconstituted thymus organ culture is based on fetal thymus organ culture (FTOC). Purified thymocyte populations, from genetically modified mice or even from other species, are cultured in vitro with thymic lobes depleted of their endogenous thymocytes (by 2'-deoxyguanosine treatment) to form a new thymus. This potent and timesaving method is distinct from FTOC, which assesses development of unmodified thymic lobes, and reaggregate thymic organ culture, in which epithelial cells are separately purified before being aggregated with thymocytes.
    MeSH term(s) Animals ; Cell Culture Techniques ; Cell Separation ; Female ; Fetus ; Genetic Vectors/genetics ; Mice ; Organ Culture Techniques ; Precursor Cells, B-Lymphoid/cytology ; Precursor Cells, B-Lymphoid/metabolism ; Pregnancy ; Retroviridae/genetics ; Thymocytes/cytology ; Thymocytes/metabolism ; Thymus Gland ; Transduction, Genetic
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-2809-5_13
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  6. Article ; Online: RAG1-mediated ubiquitylation of histone H3 is required for chromosomal V(D)J recombination.

    Deng, Zimu / Liu, Haifeng / Liu, Xiaolong

    Cell research

    2015  Volume 25, Issue 2, Page(s) 181–192

    Abstract: RAG1 and RAG2 proteins are key components in V(D)J recombination. The core region of RAG1 is capable of catalyzing the recombination reaction; however, the biological function of non-core RAG1 remains largely unknown. Here, we show that in a murine-model ...

    Abstract RAG1 and RAG2 proteins are key components in V(D)J recombination. The core region of RAG1 is capable of catalyzing the recombination reaction; however, the biological function of non-core RAG1 remains largely unknown. Here, we show that in a murine-model carrying the RAG1 ring-finger conserved cysteine residue mutation (C325Y), V(D)J recombination was abrogated at the cleavage step, and this effect was accompanied by decreased mono-ubiquitylation of histone H3. Further analyses suggest that un-ubiquitylated histone H3 restrains RAG1 to the chromatin by interacting with the N-terminal 218 amino acids of RAG1. Our data provide evidence for a model in which ubiquitylation of histone H3 mediated by the ring-finger domain of RAG1 triggers the release of RAG1, thus allowing its transition into the cleavage phase. Collectively, our findings reveal that the non-core region of RAG1 facilitates chromosomal V(D)J recombination in a ubiquitylation-dependent pathway.
    MeSH term(s) Amino Acid Substitution ; Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Chromosomes/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; Female ; HEK293 Cells ; Histones/metabolism ; Homeodomain Proteins/chemistry ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Transfection ; Ubiquitination ; V(D)J Recombination/physiology
    Chemical Substances DNA-Binding Proteins ; Histones ; Homeodomain Proteins ; Rag2 protein, mouse ; Receptors, Antigen, T-Cell, alpha-beta ; RAG-1 protein (128559-51-3)
    Language English
    Publishing date 2015-02
    Publishing country England
    Document type Journal Article ; 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/cr.2015.1
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    Zs.A 5283: Show issues Location:
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  7. Article ; Online: A Defect in Thymic Tolerance Causes T Cell-Mediated Autoimmunity in a Murine Model of COPA Syndrome.

    Deng, Zimu / Law, Christopher S / Ho, Frances O / Wang, Kristin M / Jones, Kirk D / Shin, Jeoung-Sook / Shum, Anthony K

    Journal of immunology (Baltimore, Md. : 1950)

    2020  Volume 204, Issue 9, Page(s) 2360–2373

    Abstract: COPA syndrome is a recently described Mendelian autoimmune disorder caused by missense mutations in ... ...

    Abstract COPA syndrome is a recently described Mendelian autoimmune disorder caused by missense mutations in the
    MeSH term(s) Adoptive Transfer/methods ; Animals ; Autoimmunity/genetics ; Autoimmunity/immunology ; Coatomer Protein/genetics ; Coatomer Protein/immunology ; Disease Models, Animal ; Epithelial Cells/immunology ; Female ; Immune Tolerance/genetics ; Immune Tolerance/immunology ; Lung/immunology ; Lung Diseases, Interstitial/genetics ; Lung Diseases, Interstitial/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mutation/genetics ; Mutation/immunology ; Syndrome ; T-Lymphocytes/immunology ; Thymus Gland/immunology
    Chemical Substances Coatomer Protein
    Language English
    Publishing date 2020-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2000028
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    Ud II Zs.37: Show issues Location:
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  8. Article ; Online: A defect in COPI-mediated transport of STING causes immune dysregulation in COPA syndrome.

    Deng, Zimu / Chong, Zhenlu / Law, Christopher S / Mukai, Kojiro / Ho, Frances O / Martinu, Tereza / Backes, Bradley J / Eckalbar, Walter L / Taguchi, Tomohiko / Shum, Anthony K

    The Journal of experimental medicine

    2020  Volume 217, Issue 11

    Abstract: Pathogenic COPA variants cause a Mendelian syndrome of immune dysregulation with elevated type I interferon signaling. COPA is a subunit of coat protein complex I (COPI) that mediates Golgi to ER transport. Missense mutations of the COPA WD40 domain ... ...

    Abstract Pathogenic COPA variants cause a Mendelian syndrome of immune dysregulation with elevated type I interferon signaling. COPA is a subunit of coat protein complex I (COPI) that mediates Golgi to ER transport. Missense mutations of the COPA WD40 domain impair binding and sorting of proteins targeted for ER retrieval, but how this causes disease remains unknown. Given the importance of COPA in Golgi-ER transport, we speculated that type I interferon signaling in COPA syndrome involves missorting of STING. We show that a defect in COPI transport causes ligand-independent activation of STING. Furthermore, SURF4 is an adapter molecule that facilitates COPA-mediated retrieval of STING at the Golgi. Activated STING stimulates type I interferon-driven inflammation in CopaE241K/+ mice that is rescued in STING-deficient animals. Our results demonstrate that COPA maintains immune homeostasis by regulating STING transport at the Golgi. In addition, activated STING contributes to immune dysregulation in COPA syndrome and may be a new molecular target in treating the disease.
    MeSH term(s) Animals ; Coatomer Protein/genetics ; Coatomer Protein/metabolism ; Endoplasmic Reticulum/metabolism ; Fibroblasts/metabolism ; Gene Knock-In Techniques ; Golgi Apparatus/metabolism ; HEK293 Cells ; Homeostasis/immunology ; Humans ; Immune System Diseases/genetics ; Interferon Type I/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation, Missense ; Protein Transport/genetics ; Signal Transduction/genetics ; Syndrome ; Transfection
    Chemical Substances Coatomer Protein ; Interferon Type I ; Membrane Proteins ; STING1 protein, human ; SURF4 protein, human ; Sting1 protein, mouse ; Surf4 protein, mouse
    Language English
    Publishing date 2020-07-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20201045
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  9. Article: Analysis of pulmonary features and treatment approaches in the COPA syndrome.

    Tsui, Jessica L / Estrada, Oscar A / Deng, Zimu / Wang, Kristin M / Law, Christopher S / Elicker, Brett M / Jones, Kirk D / Dell, Sharon D / Gudmundsson, Gunnar / Hansdottir, Sif / Helfgott, Simon M / Volpi, Stefano / Gattorno, Marco / Waterfield, Michael R / Chan, Alice Y / Chung, Sharon A / Ley, Brett / Shum, Anthony K

    ERJ open research

    2018  Volume 4, Issue 2

    Abstract: The COPA syndrome is a monogenic, autoimmune lung and joint disorder first identified in 2015. This study sought to define the main pulmonary features of the COPA syndrome in an international cohort of patients, analyse patient responses to treatment and ...

    Abstract The COPA syndrome is a monogenic, autoimmune lung and joint disorder first identified in 2015. This study sought to define the main pulmonary features of the COPA syndrome in an international cohort of patients, analyse patient responses to treatment and highlight when genetic testing should be considered. We established a cohort of subjects (N=14) with COPA syndrome seen at multiple centres including the University of California, San Francisco, CA, USA. All subjects had one of the previously established mutations in the
    Language English
    Publishing date 2018-06-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2827830-6
    ISSN 2312-0541
    ISSN 2312-0541
    DOI 10.1183/23120541.00017-2018
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