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  1. Article ; Online: LITAF protects against pore-forming protein-induced cell death by promoting membrane repair.

    Stefani, Caroline / Bruchez, Anna M / Rosasco, Mario G / Yoshida, Anna E / Fasano, Kayla J / Levan, Paula F / Lorant, Alina / Hubbard, Nicholas W / Oberst, Andrew / Stuart, Lynda M / Lacy-Hulbert, Adam

    Science immunology

    2024  Volume 9, Issue 91, Page(s) eabq6541

    Abstract: Pore-forming toxins (PFTs) are the largest class of bacterial toxins and contribute to virulence by triggering host cell death. Vertebrates also express endogenous pore-forming proteins that induce cell death as part of host defense. To mitigate damage ... ...

    Abstract Pore-forming toxins (PFTs) are the largest class of bacterial toxins and contribute to virulence by triggering host cell death. Vertebrates also express endogenous pore-forming proteins that induce cell death as part of host defense. To mitigate damage and promote survival, cells mobilize membrane repair mechanisms to neutralize and counteract pores, but how these pathways are activated is poorly understood. Here, we use a transposon-based gene activation screen to discover pathways that counteract the cytotoxicity of the archetypal PFT
    MeSH term(s) Animals ; Cell Death ; Cell Membrane ; Pyroptosis ; Endosomes ; Bacterial Toxins
    Chemical Substances Bacterial Toxins
    Language English
    Publishing date 2024-01-05
    Publishing country United States
    Document type Journal Article
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abq6541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cutting Edge: DOCK8 Regulates a Subset of Dendritic Cells That Is Critical for the Development of Experimental Autoimmune Encephalomyelitis.

    Weliwitigoda, Asanga / Palle, Pushpalatha / Gessner, Melissa / Hubbard, Nicholas W / Oukka, Mohamed / Bettelli, Estelle

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 207, Issue 10, Page(s) 2417–2422

    Abstract: Dedicator of cytokinesis 8 (DOCK8) is a guanine nucleotide exchange factor with an essential role in cytoskeletal rearrangement, cell migration, and survival of various immune cells. Interestingly, DOCK8-deficient mice are resistant to the development of ...

    Abstract Dedicator of cytokinesis 8 (DOCK8) is a guanine nucleotide exchange factor with an essential role in cytoskeletal rearrangement, cell migration, and survival of various immune cells. Interestingly, DOCK8-deficient mice are resistant to the development of experimental autoimmune encephalomyelitis (EAE). To understand if EAE resistance in these mice results from an alteration in dendritic cell (DC) functions, we generated mice with conditional deletion of DOCK8 in DCs and observed attenuated EAE in these mice compared with control mice. Additionally, we demonstrated that DOCK8 is important for the existence of splenic conventional DC2 and lymph node migratory DCs and further established that migratory DC, rather than resident DC, are essential for the generation and proliferation of pathogenic T cell populations upon immunization with myelin Ag in adjuvant. Therefore, our data suggest that limiting migratory DCs through DOCK8 deletion and possibly other mechanisms could limit the development of CNS autoimmunity.
    MeSH term(s) Animals ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Guanine Nucleotide Exchange Factors/immunology ; Male ; Mice ; Mice, Inbred C57BL
    Chemical Substances Dock8 protein, mouse ; Guanine Nucleotide Exchange Factors
    Language English
    Publishing date 2021-10-18
    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.2001294
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.37: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 28: Show issues

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  3. Article ; Online: ADAR1 mutation causes ZBP1-dependent immunopathology.

    Hubbard, Nicholas W / Ames, Joshua M / Maurano, Megan / Chu, Lan H / Somfleth, Kim Y / Gokhale, Nandan S / Werner, Margo / Snyder, Jessica M / Lichauco, Katrina / Savan, Ram / Stetson, Daniel B / Oberst, Andrew

    Nature

    2022  Volume 607, Issue 7920, Page(s) 769–775

    Abstract: The RNA-editing enzyme ADAR1 is essential for the suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA ... ...

    Abstract The RNA-editing enzyme ADAR1 is essential for the suppression of innate immune activation and pathology caused by aberrant recognition of self-RNA, a role it carries out by disrupting the duplex structure of endogenous double-stranded RNA species
    MeSH term(s) Adenosine Deaminase/genetics ; Adenosine Deaminase/metabolism ; Animals ; Caspase 8/genetics ; Caspase 8/metabolism ; Cell Death ; Gene Deletion ; Immune System Diseases/genetics ; Immune System Diseases/metabolism ; Immune System Diseases/pathology ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Mammals/genetics ; Mutation ; Protein Kinases/deficiency ; Protein Kinases/genetics ; RNA, Double-Stranded/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/deficiency ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Signal Transduction
    Chemical Substances RNA, Double-Stranded ; RNA-Binding Proteins ; Protein Kinases (EC 2.7.-) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Caspase 8 (EC 3.4.22.-) ; Adenosine Deaminase (EC 3.5.4.4)
    Language English
    Publishing date 2022-07-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-04896-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 9: Show issues
    Zs.MO 244: Show issues

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  4. Article ; Online: Intratumoral activation of the necroptotic pathway components RIPK1 and RIPK3 potentiates antitumor immunity.

    Snyder, Annelise G / Hubbard, Nicholas W / Messmer, Michelle N / Kofman, Sigal B / Hagan, Cassidy E / Orozco, Susana L / Chiang, Kristy / Daniels, Brian P / Baker, David / Oberst, Andrew

    Science immunology

    2019  Volume 4, Issue 36

    Abstract: Although the signaling events that induce different forms of programmed cell death are well defined, the subsequent immune responses to dying cells in the context of cancer remain relatively unexplored. Necroptosis occurs downstream of the receptor- ... ...

    Abstract Although the signaling events that induce different forms of programmed cell death are well defined, the subsequent immune responses to dying cells in the context of cancer remain relatively unexplored. Necroptosis occurs downstream of the receptor-interacting protein kinases RIPK1 and RIPK3, whose activation leads to lytic cell death accompanied by de novo production of proinflammatory mediators. Here, we show that ectopic introduction of necroptotic cells to the tumor microenvironment promotes BATF3
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; Dendritic Cells/immunology ; Dependovirus/genetics ; Female ; HEK293 Cells ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; NIH 3T3 Cells ; Necroptosis/immunology ; Neoplasms/immunology ; Programmed Cell Death 1 Receptor/immunology ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/immunology ; Signal Transduction ; Tumor Microenvironment/immunology
    Chemical Substances Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
    Language English
    Publishing date 2019-06-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.aaw2004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Rapid immune reconstitution of SCID-X1 canines after G-CSF/AMD3100 mobilization and in vivo gene therapy.

    Humbert, Olivier / Chan, Frieda / Rajawat, Yogendra S / Torgerson, Troy R / Burtner, Christopher R / Hubbard, Nicholas W / Humphrys, Daniel / Norgaard, Zachary K / O'Donnell, Patricia / Adair, Jennifer E / Trobridge, Grant D / Scharenberg, Andrew M / Felsburg, Peter J / Rawlings, David J / Kiem, Hans-Peter

    Blood advances

    2018  Volume 2, Issue 9, Page(s) 987–999

    Abstract: Hematopoietic stem-cell gene therapy is a promising treatment of X-linked severe combined immunodeficiency disease (SCID-X1), but currently, it requires recipient conditioning, extensive cell manipulation, and sophisticated facilities. With these ... ...

    Abstract Hematopoietic stem-cell gene therapy is a promising treatment of X-linked severe combined immunodeficiency disease (SCID-X1), but currently, it requires recipient conditioning, extensive cell manipulation, and sophisticated facilities. With these limitations in mind, we explored a simpler therapeutic approach to SCID-X1 treatment by direct IV administration of foamy virus (FV) vectors in the canine model. FV vectors were used because they have a favorable integration site profile and are resistant to serum inactivation. Here, we show improved efficacy of our in vivo gene therapy platform by mobilization with granulocyte colony-stimulating factor (G-CSF) and AMD3100 before injection of an optimized FV vector incorporating the human phosphoglycerate kinase enhancerless promoter. G-CSF/AMD3100 mobilization before FV vector delivery accelerated kinetics of CD3
    MeSH term(s) Animals ; Benzylamines ; CD4-CD8 Ratio ; Cyclams ; Disease Models, Animal ; Dog Diseases/blood ; Dog Diseases/genetics ; Dog Diseases/therapy ; Dogs ; Genetic Therapy ; Genetic Vectors/pharmacology ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Mobilization ; Heterocyclic Compounds/pharmacology ; Humans ; Phosphoglycerate Kinase/genetics ; Spumavirus ; X-Linked Combined Immunodeficiency Diseases/blood ; X-Linked Combined Immunodeficiency Diseases/genetics ; X-Linked Combined Immunodeficiency Diseases/therapy ; X-Linked Combined Immunodeficiency Diseases/veterinary
    Chemical Substances Benzylamines ; Cyclams ; Heterocyclic Compounds ; Granulocyte Colony-Stimulating Factor (143011-72-7) ; Phosphoglycerate Kinase (EC 2.7.2.3) ; plerixafor (S915P5499N)
    Language English
    Publishing date 2018-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2018016451
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 7153: Show issues Location:
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