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  1. Article ; Online: B cell-intrinsic requirement for WNK1 kinase in antibody responses in mice.

    Hayward, Darryl A / Vanes, Lesley / Wissmann, Stefanie / Sivapatham, Sujana / Hartweger, Harald / Biggs O'May, Joshua / de Boer, Leonard L / Mitter, Richard / Köchl, Robert / Stein, Jens V / Tybulewicz, Victor L J

    The Journal of experimental medicine

    2023  Volume 220, Issue 3

    Abstract: Migration and adhesion play critical roles in B cells, regulating recirculation between lymphoid organs, migration within lymphoid tissue, and interaction with CD4+ T cells. However, there is limited knowledge of how B cells integrate chemokine receptor ... ...

    Abstract Migration and adhesion play critical roles in B cells, regulating recirculation between lymphoid organs, migration within lymphoid tissue, and interaction with CD4+ T cells. However, there is limited knowledge of how B cells integrate chemokine receptor and integrin signaling with B cell activation to generate efficient humoral responses. Here, we show that the WNK1 kinase, a regulator of migration and adhesion, is essential in B cells for T-dependent and -independent antibody responses. We demonstrate that WNK1 transduces signals from the BCR, CXCR5, and CD40, and using intravital imaging, we show that WNK1 regulates migration of naive and activated B cells, and their interactions with T cells. Unexpectedly, we show that WNK1 is required for BCR- and CD40-induced proliferation, acting through the OXSR1 and STK39 kinases, and for efficient B cell-T cell collaboration in vivo. Thus, WNK1 is critical for humoral immune responses, by regulating B cell migration, adhesion, and T cell-dependent activation.
    MeSH term(s) Mice ; Animals ; Antibody Formation ; B-Lymphocytes ; Lymphoid Tissue ; Signal Transduction ; CD4-Positive T-Lymphocytes ; CD40 Antigens/metabolism ; WNK Lysine-Deficient Protein Kinase 1/metabolism
    Chemical Substances CD40 Antigens ; Wnk1 protein, mouse (EC 2.7.11.1) ; WNK Lysine-Deficient Protein Kinase 1 (EC 2.7.11.1)
    Language English
    Publishing date 2023-01-20
    Publishing country United States
    Document type Journal Article ; 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.20211827
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  2. Article ; Online: T cell migration requires ion and water influx to regulate actin polymerization.

    de Boer, Leonard L / Vanes, Lesley / Melgrati, Serena / Biggs O'May, Joshua / Hayward, Darryl / Driscoll, Paul C / Day, Jason / Griffiths, Alexander / Magueta, Renata / Morrell, Alexander / MacRae, James I / Köchl, Robert / Tybulewicz, Victor L J

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 7844

    Abstract: Migration of T cells is essential for their ability to mount immune responses. Chemokine-induced T cell migration requires WNK1, a kinase that regulates ion influx into the cell. However, it is not known why ion entry is necessary for T cell movement. ... ...

    Abstract Migration of T cells is essential for their ability to mount immune responses. Chemokine-induced T cell migration requires WNK1, a kinase that regulates ion influx into the cell. However, it is not known why ion entry is necessary for T cell movement. Here we show that signaling from the chemokine receptor CCR7 leads to activation of WNK1 and its downstream pathway at the leading edge of migrating CD4
    MeSH term(s) Actins/metabolism ; Polymerization ; Cell Movement/physiology ; Actin Cytoskeleton/metabolism ; Signal Transduction/physiology
    Chemical Substances Actins
    Language English
    Publishing date 2023-12-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-43423-8
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  3. Article: Lessons learned from the mechanisms of posttraumatic inflammation extrapolated to the inflammatory response in COVID-19: a review.

    Teuben, Michel P J / Pfeifer, Roman / Teuber, Henrik / De Boer, Leonard L / Halvachizadeh, Sascha / Shehu, Alba / Pape, Hans-Christoph

    Patient safety in surgery

    2020  Volume 14, Page(s) 28

    Abstract: Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in ... ...

    Abstract Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in severe trauma cases. This review compares pathophysiological and therapeutic principles of severely injured trauma patients and severe coronavirus disease 2019 (COVID-19). The development of sequential organ failure in trauma parallels deterioration seen in severe COVID-19. Based on established pathophysiological models in the field of trauma, two complementary pathways of disease progression into severe COVID-19 have been identified. Furthermore, the transition from local contained disease into systemic and remote inflammation has been addressed. More specifically, the traumatology concept of sequential insults ('hits') resulting in immune dysregulation, is applied to COVID-19 disease progression modelling. Finally, similarities in post-insult humoral and cellular immune responses to severe trauma and severe COVID-19 are described. To minimize additional 'hits' to COVID-19 patients, we suggest postponing all elective surgery in endemic areas. Based on traumatology experience, we propose that immunoprotective protocols including lung protective ventilation, optimal thrombosis prophylaxis, secondary infection prevention and calculated antibiotic therapy are likely also beneficial in the treatment of SARS-CoV-2 infections. Finally, rising SARS-CoV-2 infection and mortality rates mandate exploration of out-of-the box treatment concepts, including experimental therapies designed for trauma care.
    Keywords covid19
    Language English
    Publishing date 2020-07-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2409244-7
    ISSN 1754-9493
    ISSN 1754-9493
    DOI 10.1186/s13037-020-00253-7
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  4. Article ; Online: Lessons learned from the mechanisms of posttraumatic inflammation extrapolated to the inflammatory response in COVID-19

    Teuben, Michel P. J. / Pfeifer, Roman / Teuber, Henrik / De Boer, Leonard L. / Halvachizadeh, Sascha / Shehu, Alba / Pape, Hans-Christoph

    Patient Safety in Surgery

    a review

    2020  Volume 14, Issue 1

    Keywords Anesthesiology and Pain Medicine ; Surgery ; Orthopedics and Sports Medicine ; covid19
    Language English
    Publisher Springer Science and Business Media LLC
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2409244-7
    ISSN 1754-9493
    ISSN 1754-9493
    DOI 10.1186/s13037-020-00253-7
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  5. Article: Lessons learned from the mechanisms of posttraumatic inflammation extrapolated to the inflammatory response in COVID-19: A review

    Teuben, Michel P. J. / Pfeifer, Roman / Teuber, Henrik / De Boer, Leonard L. / Halvachizadeh, Sascha / Shehu, Alba / Pape, Hans-Christoph

    Patient Saf. Surg.

    Abstract: Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in ... ...

    Abstract Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in severe trauma cases. This review compares pathophysiological and therapeutic principles of severely injured trauma patients and severe coronavirus disease 2019 (COVID-19). The development of sequential organ failure in trauma parallels deterioration seen in severe COVID-19. Based on established pathophysiological models in the field of trauma, two complementary pathways of disease progression into severe COVID-19 have been identified. Furthermore, the transition from local contained disease into systemic and remote inflammation has been addressed. More specifically, the traumatology concept of sequential insults ('hits') resulting in immune dysregulation, is applied to COVID-19 disease progression modelling. Finally, similarities in post-insult humoral and cellular immune responses to severe trauma and severe COVID-19 are described. To minimize additional 'hits' to COVID-19 patients, we suggest postponing all elective surgery in endemic areas. Based on traumatology experience, we propose that immunoprotective protocols including lung protective ventilation, optimal thrombosis prophylaxis, secondary infection prevention and calculated antibiotic therapy are likely also beneficial in the treatment of SARS-CoV-2 infections. Finally, rising SARS-CoV-2 infection and mortality rates mandate exploration of out-of-the box treatment concepts, including experimental therapies designed for trauma care.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #637200
    Database COVID19

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  6. Article ; Online: Lessons learned from the mechanisms of posttraumatic inflammation extrapolated to the inflammatory response in COVID-19

    Teuben, Michel P J / Pfeifer, Roman / Teuber, Henrik / De Boer, Leonard L / Halvachizadeh, Sascha / Shehu, Alba / Pape, Hans-Christoph

    Teuben, Michel P J; Pfeifer, Roman; Teuber, Henrik; De Boer, Leonard L; Halvachizadeh, Sascha; Shehu, Alba; Pape, Hans-Christoph (2020). Lessons learned from the mechanisms of posttraumatic inflammation extrapolated to the inflammatory response in COVID-19: a review. Patient Safety in Surgery, 14:28.

    a review

    2020  

    Abstract: Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in ... ...

    Abstract Up to 20% of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) patients develop severe inflammatory complications with diffuse pulmonary inflammation, reflecting acute respiratory distress syndrome (ARDS). A similar clinical profile occurs in severe trauma cases. This review compares pathophysiological and therapeutic principles of severely injured trauma patients and severe coronavirus disease 2019 (COVID-19). The development of sequential organ failure in trauma parallels deterioration seen in severe COVID-19. Based on established pathophysiological models in the field of trauma, two complementary pathways of disease progression into severe COVID-19 have been identified. Furthermore, the transition from local contained disease into systemic and remote inflammation has been addressed. More specifically, the traumatology concept of sequential insults ('hits') resulting in immune dysregulation, is applied to COVID-19 disease progression modelling. Finally, similarities in post-insult humoral and cellular immune responses to severe trauma and severe COVID-19 are described. To minimize additional 'hits' to COVID-19 patients, we suggest postponing all elective surgery in endemic areas. Based on traumatology experience, we propose that immunoprotective protocols including lung protective ventilation, optimal thrombosis prophylaxis, secondary infection prevention and calculated antibiotic therapy are likely also beneficial in the treatment of SARS-CoV-2 infections. Finally, rising SARS-CoV-2 infection and mortality rates mandate exploration of out-of-the box treatment concepts, including experimental therapies designed for trauma care.
    Keywords Department of Trauma Surgery ; 610 Medicine & health ; covid19
    Subject code 610
    Language English
    Publisher BioMed Central
    Publishing country ch
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Airway persistence by the emerging multi-azole-resistant Rasamsonia argillacea complex in cystic fibrosis.

    Abdolrasouli, Alireza / Bercusson, Amelia C / Rhodes, Johanna L / Hagen, Ferry / Buil, Jochem B / Tang, Alison Y Y / de Boer, Leonard L / Shah, Anand / Milburn, Andrew J / Elborn, J Stuart / Jones, Andrew L / Meis, Jacques F / Fisher, Matthew C / Schelenz, Silke / Simmonds, Nicholas J / Armstrong-James, Darius

    Mycoses

    2018  Volume 61, Issue 9, Page(s) 665–673

    Abstract: Infections caused by Rasamsonia argillacea complex have been reported in various clinical settings. Cystic fibrosis (CF) is one of the main underlying conditions. An observational cohort study of CF patients with Rasamsonia in respiratory samples was ... ...

    Abstract Infections caused by Rasamsonia argillacea complex have been reported in various clinical settings. Cystic fibrosis (CF) is one of the main underlying conditions. An observational cohort study of CF patients with Rasamsonia in respiratory samples was conducted. Eight isolates from 6 patients were identified as R. argillacea complex and tested for antifungal susceptibility. All isolates had high MICs to voriconazole and posaconazole and low MECs to echinocandins. Four patients experienced lung function decline in the year preceding first Rasamsonia isolation. This continued in the year following first isolation in 3 out of 4 cases. Antifungal therapy was initiated in 2 patients, to which only one exhibited a clinical response. Three out of 6 patients died within 3 years of isolating Rasamsonia. Genotyping suggests that similar genotypes of Rasamsonia can persist in CF airways. Consistent with other fungi in CF, the clinical impact of airway colonisation by Rasamsonia is variable. In certain patients, Rasamsonia may be able to drive clinical decline. In others, though a clear impact on lung function may be difficult to determine, the appearance of Rasamsonia acts as a marker of disease severity. In others it does not appear to have an obvious clinical impact on disease progression.
    MeSH term(s) Adult ; Antifungal Agents/pharmacology ; Azoles/pharmacology ; Child ; Cohort Studies ; Communicable Diseases, Emerging/microbiology ; Cystic Fibrosis/complications ; Drug Resistance, Fungal ; Echinocandins/pharmacology ; Eurotiales/classification ; Eurotiales/drug effects ; Eurotiales/genetics ; Eurotiales/isolation & purification ; Female ; Genotype ; Genotyping Techniques ; Humans ; Lung Diseases, Fungal/microbiology ; Male ; Microbial Sensitivity Tests ; Middle Aged ; Mycological Typing Techniques ; Young Adult
    Chemical Substances Antifungal Agents ; Azoles ; Echinocandins
    Language English
    Publishing date 2018-06-20
    Publishing country Germany
    Document type Journal Article ; Observational Study
    ZDB-ID 392487-7
    ISSN 1439-0507 ; 0933-7407
    ISSN (online) 1439-0507
    ISSN 0933-7407
    DOI 10.1111/myc.12789
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    Ud II Zs.176: Show issues Location:
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