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  1. Article ; Online: Aspecific binding of anti-NK1.1 antibodies on myeloid cells in an experimental model for malaria-associated acute respiratory distress syndrome.

    Pollenus, Emilie / Prenen, Fran / Possemiers, Hendrik / Knoops, Sofie / Mitera, Tania / Lamote, Jochen / De Visscher, Amber / Vandermosten, Leen / Pham, Thao-Thy / Matthys, Patrick / Van den Steen, Philippe E

    Malaria journal

    2024  Volume 23, Issue 1, Page(s) 110

    Abstract: Background: Conventional natural killer (cNK) cells play an important role in the innate immune response by directly killing infected and malignant cells and by producing pro- and anti-inflammatory cytokines. Studies on their role in malaria and its ... ...

    Abstract Background: Conventional natural killer (cNK) cells play an important role in the innate immune response by directly killing infected and malignant cells and by producing pro- and anti-inflammatory cytokines. Studies on their role in malaria and its complications have resulted in conflicting results.
    Methods: Using the commonly used anti-NK1.1 depletion antibodies (PK136) in an in-house optimized experimental model for malaria-associated acute respiratory distress syndrome (MA-ARDS), the role of cNK cells was investigated. Moreover, flow cytometry was performed to characterize different NK cell populations.
    Results: While cNK cells were found to be dispensable in the development of MA-ARDS, the appearance of a NK1.1
    Conclusion: cNK cells are dispensable in the development of experimental MA-ARDS. Moreover, careful flow cytometric analysis, with a critical mindset in relation to potential aspecific binding despite the use of commercially available Fc blocking reagents, is critical to avoid misinterpretation of the results.
    MeSH term(s) Mice ; Animals ; Mice, Inbred C57BL ; Respiratory Distress Syndrome/pathology ; Killer Cells, Natural ; Myeloid Cells/pathology ; Malaria/complications
    Language English
    Publishing date 2024-04-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2091229-8
    ISSN 1475-2875 ; 1475-2875
    ISSN (online) 1475-2875
    ISSN 1475-2875
    DOI 10.1186/s12936-024-04944-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Role for Granulocyte Colony-Stimulating Factor in Neutrophilic Extramedullary Myelopoiesis in a Murine Model of Systemic Juvenile Idiopathic Arthritis.

    Malengier-Devlies, Bert / Bernaerts, Eline / Ahmadzadeh, Kourosh / Filtjens, Jessica / Vandenhaute, Jessica / Boeckx, Bram / Burton, Oliver / De Visscher, Amber / Mitera, Tania / Berghmans, Nele / Verbeke, Geert / Liston, Adrian / Lambrechts, Diether / Proost, Paul / Wouters, Carine / Matthys, Patrick

    Arthritis & rheumatology (Hoboken, N.J.)

    2022  Volume 74, Issue 7, Page(s) 1257–1270

    Abstract: Objective: Systemic juvenile idiopathic arthritis (JIA) is a systemic inflammatory disease with childhood onset. Systemic JIA is associated with neutrophilia, including immature granulocytes, potentially driven by the growth factor granulocyte-colony ... ...

    Abstract Objective: Systemic juvenile idiopathic arthritis (JIA) is a systemic inflammatory disease with childhood onset. Systemic JIA is associated with neutrophilia, including immature granulocytes, potentially driven by the growth factor granulocyte-colony stimulating factor (G-CSF). This study was undertaken to investigate the role of G-CSF in the pathology of systemic JIA.
    Methods: Injection of Freund's complete adjuvant (CFA) in BALB/c mice induces mild inflammation and neutrophilia in wild-type (WT) mice and a more pronounced disease, reminiscent to that of JIA patients, in interferon-γ-knockout (IFNγ-KO) mice. Extramedullary myelopoiesis was studied in CFA-immunized mice by single-cell RNA sequencing, and the effect of G-CSF receptor (G-CSFR) blockage on neutrophil development and systemic JIA pathology was evaluated. Additionally, plasma G-CSF levels were measured in patients.
    Results: Both in systemic JIA patients and in a corresponding mouse model, plasma G-CSF levels were increased. In the mouse model, we demonstrated that G-CSF is responsible for the observed neutrophilia and extramedullary myelopoiesis and the induction of immature neutrophils and myeloid-derived suppressor-like cells. Administration of a G-CSFR antagonizing antibody blocked the maturation and differentiation of neutrophils in CFA-immunized mice. In IFNγ-KO mice, treatment was associated with almost complete inhibition of arthritis due to reduced neutrophilia and osteoclast formation. Disease symptoms were ameliorated, but slight increases in interleukin-6 (IL-6), tumor necrosis factor, and IL-17 were detected upon G-CSFR inhibition in the IFNγ-KO mice, and were associated with mild increases in weight loss, tail damage, and immature red blood cells.
    Conclusion: We describe the role of G-CSF in a mouse model of systemic JIA and suggest an important role for G-CSF-induced myelopoiesis and neutrophilia in regulating the development of arthritis.
    MeSH term(s) Animals ; Arthritis, Juvenile/immunology ; Disease Models, Animal ; Granulocyte Colony-Stimulating Factor/immunology ; Interferon-gamma/genetics ; Mice ; Mice, Inbred BALB C ; Myelopoiesis ; Neutrophils/metabolism
    Chemical Substances Granulocyte Colony-Stimulating Factor (143011-72-7) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2022-05-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 24: 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)

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  3. Article ; Online: Homozygous DBF4 mutation as a cause of severe congenital neutropenia.

    Willemsen, Mathijs / Barber, John S / Nieuwenhove, Erika Van / Staels, Frederik / Gerbaux, Margaux / Neumann, Julika / Prezzemolo, Teresa / Pasciuto, Emanuela / Lagou, Vasiliki / Boeckx, Nancy / Filtjens, Jessica / De Visscher, Amber / Matthys, Patrick / Schrijvers, Rik / Tousseyn, Thomas / O'Driscoll, Mark / Bucciol, Giorgia / Schlenner, Susan / Meyts, Isabelle /
    Humblet-Baron, Stephanie / Liston, Adrian

    The Journal of allergy and clinical immunology

    2023  Volume 152, Issue 1, Page(s) 266–277

    Abstract: Background: Severe congenital neutropenia presents with recurrent infections early in life as a result of arrested granulopoiesis. Multiple genetic defects are known to block granulocyte differentiation; however, a genetic cause remains unknown in ... ...

    Abstract Background: Severe congenital neutropenia presents with recurrent infections early in life as a result of arrested granulopoiesis. Multiple genetic defects are known to block granulocyte differentiation; however, a genetic cause remains unknown in approximately 40% of cases.
    Objective: We aimed to characterize a patient with severe congenital neutropenia and syndromic features without a genetic diagnosis.
    Methods: Whole exome sequencing results were validated using flow cytometry, Western blotting, coimmunoprecipitation, quantitative PCR, cell cycle and proliferation analysis of lymphocytes and fibroblasts and granulocytic differentiation of primary CD34
    Results: We identified a homozygous missense mutation in DBF4 in a patient with mild extra-uterine growth retardation, facial dysmorphism and severe congenital neutropenia. DBF4 is the regulatory subunit of the CDC7 kinase, together known as DBF4-dependent kinase (DDK), the complex essential for DNA replication initiation. The DBF4 variant demonstrated impaired ability to bind CDC7, resulting in decreased DDK-mediated phosphorylation, defective S-phase entry and progression and impaired differentiation of granulocytes associated with activation of the p53-p21 pathway. The introduction of wild-type DBF4 into patient CD34
    Conclusion: Hypomorphic DBF4 mutation causes autosomal-recessive severe congenital neutropenia with syndromic features.
    MeSH term(s) Humans ; Cell Cycle Proteins/genetics ; Protein Serine-Threonine Kinases/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Mutation ; Phosphorylation
    Chemical Substances Cell Cycle Proteins ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Saccharomyces cerevisiae Proteins ; CDC7 protein, human (EC 2.7.1.-) ; DBF4 protein, human
    Language English
    Publishing date 2023-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2023.02.016
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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.92: 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)

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  4. Article ; Online: Severe COVID-19 patients display hyper-activated NK cells and NK cell-platelet aggregates.

    Malengier-Devlies, Bert / Filtjens, Jessica / Ahmadzadeh, Kourosh / Boeckx, Bram / Vandenhaute, Jessica / De Visscher, Amber / Bernaerts, Eline / Mitera, Tania / Jacobs, Cato / Vanderbeke, Lore / Van Mol, Pierre / Van Herck, Yannick / Hermans, Greet / Meersseman, Philippe / Wilmer, Alexander / Gouwy, Mieke / Garg, Abhishek D / Humblet-Baron, Stephanie / De Smet, Frederik /
    Martinod, Kimberly / Wauters, Els / Proost, Paul / Wouters, Carine / Leclercq, Georges / Lambrechts, Diether / Wauters, Joost / Matthys, Patrick

    Frontiers in immunology

    2022  Volume 13, Page(s) 861251

    Abstract: COVID-19 is characterised by a broad spectrum of clinical and pathological features. Natural killer (NK) cells play an important role in innate immune responses to viral infections. Here, we analysed the phenotype and activity of NK cells in the blood of ...

    Abstract COVID-19 is characterised by a broad spectrum of clinical and pathological features. Natural killer (NK) cells play an important role in innate immune responses to viral infections. Here, we analysed the phenotype and activity of NK cells in the blood of COVID-19 patients using flow cytometry, single-cell RNA-sequencing (scRNA-seq), and a cytotoxic killing assay. In the plasma of patients, we quantified the main cytokines and chemokines. Our cohort comprises COVID-19 patients hospitalised in a low-care ward unit (WARD), patients with severe COVID-19 disease symptoms hospitalised in intensive care units (ICU), and post-COVID-19 patients, who were discharged from hospital six weeks earlier. NK cells from hospitalised COVID-19 patients displayed an activated phenotype with substantial differences between WARD and ICU patients and the timing when samples were taken post-onset of symptoms. While NK cells from COVID-19 patients at an early stage of infection showed increased expression of the cytotoxic molecules perforin and granzyme A and B, NK cells from patients at later stages of COVID-19 presented enhanced levels of IFN-γ and TNF-α which were measured
    MeSH term(s) Humans ; Granzymes/metabolism ; COVID-19 ; Perforin/metabolism ; Interleukin-15/metabolism ; Interleukin-18/metabolism ; SARS-CoV-2 ; Tumor Necrosis Factor-alpha/metabolism ; Blood Platelets/metabolism ; Integrin alpha1/metabolism ; Killer Cells, Natural ; Cytokines/metabolism ; Chemokines/metabolism ; Interleukin-12/metabolism ; Antiviral Agents/metabolism ; RNA/metabolism
    Chemical Substances Granzymes (EC 3.4.21.-) ; Perforin (126465-35-8) ; Interleukin-15 ; Interleukin-18 ; Tumor Necrosis Factor-alpha ; Integrin alpha1 ; Cytokines ; Chemokines ; Interleukin-12 (187348-17-0) ; Antiviral Agents ; RNA (63231-63-0)
    Language English
    Publishing date 2022-10-05
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.861251
    Database MEDical Literature Analysis and Retrieval System OnLINE

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