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  1. AU="Ashwin, Helen"
  2. AU="Skeldon, Alexander"
  3. AU="Robles, Ignacio"
  4. AU="Karla Correia Lima Miranda"
  5. AU="Benaim, G"
  6. AU="Bongers, Coen CWG"
  7. AU="Demontis, Ditte"
  8. AU="Cheng, Risheng"
  9. AU="Mendoza, Ismael Ballesteros"
  10. AU=Du Yin AU=Du Yin
  11. AU="Du, Dan-yu"
  12. AU="Collier, John L"
  13. AU="Min, Ai-Lian"
  14. AU="Chen, Jingyuan"
  15. AU="Salama, Asmaa"
  16. AU=Johnson R
  17. AU="Straathof, Karin"
  18. AU="Scanlon, Robert"
  19. AU="de la Fuente, M"
  20. AU="Li, Hezhang"
  21. AU="Portillo, María P."
  22. AU="Winter, Theresa"
  23. AU="Antoine Fakhry Abdelmassih"
  24. AU=Barazzoni Rocco
  25. AU="Yuan, Mingyang"

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  1. Artikel ; Online: Downregulation of MALAT1 is a hallmark of tissue and peripheral proliferative T cells in COVID-19.

    Dey, Shoumit / Ashwin, Helen / Milross, Luke / Hunter, Bethany / Majo, Joaquim / Filby, Andrew J / Fisher, Andrew J / Kaye, Paul M / Lagos, Dimitris

    Clinical and experimental immunology

    2023  Band 212, Heft 3, Seite(n) 262–275

    Abstract: T cells play key protective but also pathogenic roles in COVID-19. We studied the expression of long non-coding RNAs (lncRNAs) in COVID-19 T-cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic ... ...

    Abstract T cells play key protective but also pathogenic roles in COVID-19. We studied the expression of long non-coding RNAs (lncRNAs) in COVID-19 T-cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non-coding RNA MALAT1 was the most highly transcribed lncRNA in T cells, with Th1 cells demonstrating the lowest and CD8+ resident memory cells the highest MALAT1 expression, amongst CD4+ and CD8+ T-cells populations, respectively. We then identified gene signatures that covaried with MALAT1 in single T cells. A significantly higher number of transcripts correlated negatively with MALAT1 than those that correlated. Enriched functional annotations of the MALAT1- anti-correlating gene signature included processes associated with T-cell activation such as cell division, oxidative phosphorylation, and response to cytokine. The MALAT1 anti-correlating gene signature shared by both CD4+ and CD8+ T-cells marked dividing T cells in both the lung and blood of COVID-19 patients. Focussing on the tissue, we used an independent patient cohort of post-mortem COVID-19 lung samples and demonstrated that MALAT1 suppression was indeed a marker of MKI67+ proliferating CD8+ T cells. Our results reveal MALAT1 suppression and its associated gene signature are a hallmark of human proliferating T cells.
    Mesh-Begriff(e) Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Down-Regulation ; Cell Proliferation/genetics ; COVID-19/genetics ; CD8-Positive T-Lymphocytes/metabolism
    Chemische Substanzen RNA, Long Noncoding
    Sprache Englisch
    Erscheinungsdatum 2023-03-03
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad034
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  2. Artikel ; Online: Dissecting pathways to thrombocytopenia in a mouse model of visceral leishmaniasis.

    Rani, Gulab Fatima / Preham, Olivier / Ashwin, Helen / Brown, Najmeeyah / Hitchcock, Ian S / Kaye, Paul M

    Blood advances

    2021  Band 5, Heft 6, Seite(n) 1627–1637

    Abstract: Visceral leishmaniasis is an important yet neglected parasitic disease caused by infection with Leishmania donovani or L infantum. Disease manifestations include fever, weight loss, hepatosplenomegaly, immune dysregulation, and extensive hematological ... ...

    Abstract Visceral leishmaniasis is an important yet neglected parasitic disease caused by infection with Leishmania donovani or L infantum. Disease manifestations include fever, weight loss, hepatosplenomegaly, immune dysregulation, and extensive hematological complications. Thrombocytopenia is a dominant hematological feature seen in both humans and experimental models, but the mechanisms behind this infection-driven thrombocytopenia remain poorly understood. Using a murine model of experimental visceral leishmaniasis (EVL), we demonstrated a progressive decrease in platelets from day 14 after infection, culminating in severe thrombocytopenia by day 28. Plasma thrombopoietin (TPO) levels were reduced in infected mice, at least in part because of the alterations in the liver microenvironment associated with granulomatous inflammation. Bone marrow (BM) megakaryocyte cytoplasmic maturation was significantly reduced. In addition to a production deficit, we identified significant increases in platelet clearance. L donovani-infected splenectomized mice were protected from thrombocytopenia compared with sham operated infected mice and had a greater response to exogenous TPO. Furthermore, infection led to higher levels of platelet opsonization and desialylation, both associated with platelet clearance in spleen and liver, respectively. Critically, these changes could be reversed rapidly by drug treatment to reduce parasite load or by administration of TPO agonists. In summary, our findings demonstrate that the mechanisms underpinning thrombocytopenia in EVL are multifactorial and reversible, with no obvious residual damage to the BM microenvironment.
    Mesh-Begriff(e) Animals ; Disease Models, Animal ; Leishmaniasis, Visceral/complications ; Leishmaniasis, Visceral/drug therapy ; Megakaryocytes ; Mice ; Thrombocytopenia ; Thrombopoietin
    Chemische Substanzen Thrombopoietin (9014-42-0)
    Sprache Englisch
    Erscheinungsdatum 2021-03-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2020004082
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Hematological consequences of malaria in mice previously treated for visceral leishmaniasis.

    Rani, Gulab Fatima / Ashwin, Helen / Brown, Najmeeyah / Hitchcock, Ian S / Kaye, Paul M

    Wellcome open research

    2021  Band 6, Seite(n) 83

    Abstract: ... ...

    Abstract Background
    Sprache Englisch
    Erscheinungsdatum 2021-06-18
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 2398-502X
    ISSN 2398-502X
    DOI 10.12688/wellcomeopenres.16629.2
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  4. Artikel ; Online: Down-regulation of MALAT1 is a hallmark of tissue and peripheral proliferative T cells in COVID-19

    Dey, Shoumit / Ashwin, Helen / Milross, Luke / Hunter, Bethany / Majo, Joaquim / Filby, Andrew J / Fisher, Andrew J / Kaye, Paul M. / Lagos, Dimitris

    medRxiv

    Abstract: T cells play key protective but also pathogenic roles in COVID-19. We studied expression of long non-coding RNAs (lncRNAs) in COVID-19 T cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non- ... ...

    Abstract T cells play key protective but also pathogenic roles in COVID-19. We studied expression of long non-coding RNAs (lncRNAs) in COVID-19 T cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non-coding RNA MALAT1 was the most highly transcribed lncRNA in T cells, with Th1 cells demonstrating the lowest and CD8+ resident memory cells the highest MALAT1 expression, amongst CD4+ and CD8+ T cells populations, respectively. We then identified gene signatures that covaried with MALAT1 in single T cells. A significantly higher number of transcripts correlated negatively with MALAT1 than those that correlated. Enriched functional annotations of the MALAT1- anti-correlating gene signature included processes associated with T cell activation such as cell division, oxidative phosphorylation and response to cytokine. The MALAT1 anti-correlating gene signature shared by both CD4+ and CD8+ T cells marked dividing T cells in both lung and blood of COVID-19 patients. Focussing on the tissue, we used an independent patient cohort of post-mortem COVID-19 lung samples and demonstrated that MALAT1 suppression was indeed a marker of MKI67+ proliferating CD8+ T cells. Our results reveal MALAT1 suppression and its associated gene signature are a hallmark of human proliferating T cells.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2023-01-07
    Verlag Cold Spring Harbor Laboratory Press
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2023.01.06.23284229
    Datenquelle COVID19

    Volltext online

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  5. Artikel ; Online: Down-regulation of MALAT1 is a hallmark of tissue and peripheral proliferative T cells in COVID-19

    Dey, Shoumit / Ashwin, Helen / Milross, Luke / Hunter, Bethany / Maho, Joaquim / Filby, Andrew J / Fisher, Andrew J / Kaye, Paul M / Lagos, Dimitris

    medRxiv

    Abstract: T cells play key protective but also pathogenic roles in COVID-19. We studied expression of long non-coding RNAs (lncRNAs) in COVID-19 T cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non- ... ...

    Abstract T cells play key protective but also pathogenic roles in COVID-19. We studied expression of long non-coding RNAs (lncRNAs) in COVID-19 T cell transcriptomes by integrating previously published single-cell RNA sequencing datasets. The long intergenic non-coding RNA MALAT1 was the most highly transcribed lncRNA in T cells, with Th1 cells demonstrating the lowest and CD8+ resident memory cells the highest MALAT1 expression, amongst CD4+ and CD8+ T cells populations, respectively. We then identified gene signatures that covaried with MALAT1 in single T cells. A significantly higher number of transcripts correlated negatively with MALAT1 than those that correlated. Enriched functional annotations of the MALAT1- anti-correlating gene signature included processes associated with T cell activation such as cell division, oxidative phosphorylation and response to cytokine. The MALAT1 anti-correlating gene signature shared by both CD4+ and CD8+ T cells marked dividing T cells in both lung and blood of COVID-19 patients. Focussing on the tissue, we used an independent patient cohort of post-mortem COVID-19 lung samples and demonstrated that MALAT1 suppression was indeed a marker of MKI67+ proliferating CD8+ T cells. Our results reveal MALAT1 suppression and its associated gene signature are a hallmark of human proliferating T cells.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2023-01-07
    Verlag Cold Spring Harbor Laboratory Press
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2023.01.06.23284229
    Datenquelle COVID19

    Volltext online

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  6. Artikel ; Online: Identification of a protein expression signature distinguishing early from organising diffuse alveolar damage in COVID-19 patients.

    Ashwin, Helen / Milross, Luke / Wilson, Julie / Majo, Joaquim / Hang Lee, Jimmy Tsz / Calder, Grant / Hunter, Bethany / James, Sally / Lagos, Dimitris / Signoret, Nathalie / Filby, Andrew / Bayraktar, Omer Ali / Fisher, Andrew J / Kaye, Paul M

    Journal of clinical pathology

    2023  Band 76, Heft 8, Seite(n) 561–565

    Abstract: Diffuse alveolar damage (DAD) is the histological expression of acute respiratory distress syndrome and characterises lung pathology due to infection with SARS-CoV-2, and other respiratory pathogens of clinical significance. DAD reflects a time-dependent ...

    Abstract Diffuse alveolar damage (DAD) is the histological expression of acute respiratory distress syndrome and characterises lung pathology due to infection with SARS-CoV-2, and other respiratory pathogens of clinical significance. DAD reflects a time-dependent immunopathological process, progressing from an early/exudative stage through to an organising/fibrotic stage, yet within an individual these different stages of DAD may coexist. Understanding the progression of DAD is central to the development of new therapeutics to limit progressive lung damage. Here, we applied highly multiplexed spatial protein profiling to autopsy lung tissues derived from 27 patients who died from COVID-19 and identified a protein signature (ARG1, CD127, GZMB, IDO1, Ki67, phospho-PRAS40 (T246) and VISTA) that distinguishes early DAD from late DAD with good predictive accuracy. These proteins warrant further investigation as potential regulators of DAD progression.
    Mesh-Begriff(e) Humans ; COVID-19/diagnosis ; COVID-19/pathology ; SARS-CoV-2 ; Lung/pathology ; Respiratory Distress Syndrome/pathology ; Autopsy
    Sprache Englisch
    Erscheinungsdatum 2023-03-09
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 80261-x
    ISSN 1472-4146 ; 0021-9746
    ISSN (online) 1472-4146
    ISSN 0021-9746
    DOI 10.1136/jcp-2023-208771
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Spatial Point Pattern Analysis Identifies Mechanisms Shaping the Skin Parasite Landscape in

    Doehl, Johannes S P / Ashwin, Helen / Brown, Najmeeyah / Romano, Audrey / Carmichael, Samuel / Pitchford, Jon W / Kaye, Paul M

    Frontiers in immunology

    2021  Band 12, Seite(n) 795554

    Abstract: Increasing evidence suggests that in hosts infected with parasites of ... ...

    Abstract Increasing evidence suggests that in hosts infected with parasites of the
    Mesh-Begriff(e) Animals ; CD11 Antigens/metabolism ; Cluster Analysis ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Host-Parasite Interactions ; Image Processing, Computer-Assisted ; Insect Vectors/parasitology ; Leishmania donovani/immunology ; Leishmania donovani/pathogenicity ; Leishmaniasis, Visceral/immunology ; Leishmaniasis, Visceral/metabolism ; Leishmaniasis, Visceral/parasitology ; Leishmaniasis, Visceral/transmission ; Mannose Receptor/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Confocal ; Microscopy, Fluorescence ; Models, Theoretical ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Myeloid Cells/parasitology ; Phlebotomus/parasitology ; Skin/immunology ; Skin/metabolism ; Skin/parasitology ; Spatial Analysis ; Mice
    Chemische Substanzen CD11 Antigens ; DNA-Binding Proteins ; Itgax protein, mouse ; Mannose Receptor ; Rag2 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2021-12-16
    Erscheinungsland Switzerland
    Dokumenttyp 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.2021.795554
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Distinct lung cell signatures define the temporal evolution of diffuse alveolar damage in fatal COVID-19.

    Milross, Luke / Hunter, Bethany / McDonald, David / Merces, George / Thomson, Amanda / Hilkens, Catharien M U / Wills, John / Rees, Paul / Jiwa, Kasim / Cooper, Nigel / Majo, Joaquim / Ashwin, Helen / Duncan, Christopher J A / Kaye, Paul M / Bayraktar, Omer Ali / Filby, Andrew / Fisher, Andrew J

    EBioMedicine

    2023  Band 99, Seite(n) 104945

    Abstract: Background: Lung damage in severe COVID-19 is highly heterogeneous however studies with dedicated spatial distinction of discrete temporal phases of diffuse alveolar damage (DAD) and alternate lung injury patterns are lacking. Existing studies have also ...

    Abstract Background: Lung damage in severe COVID-19 is highly heterogeneous however studies with dedicated spatial distinction of discrete temporal phases of diffuse alveolar damage (DAD) and alternate lung injury patterns are lacking. Existing studies have also not accounted for progressive airspace obliteration in cellularity estimates. We used an imaging mass cytometry (IMC) analysis with an airspace correction step to more accurately identify the cellular immune response that underpins the heterogeneity of severe COVID-19 lung disease.
    Methods: Lung tissue was obtained at post-mortem from severe COVID-19 deaths. Pathologist-selected regions of interest (ROIs) were chosen by light microscopy representing the patho-evolutionary spectrum of DAD and alternate disease phenotypes were selected for comparison. Architecturally normal SARS-CoV-2-positive lung tissue and tissue from SARS-CoV-2-negative donors served as controls. ROIs were stained for 40 cellular protein markers and ablated using IMC before segmented cells were classified. Cell populations corrected by ROI airspace and their spatial relationships were compared across lung injury patterns.
    Findings: Forty patients (32M:8F, age: 22-98), 345 ROIs and >900k single cells were analysed. DAD progression was marked by airspace obliteration and significant increases in mononuclear phagocytes (MnPs), T and B lymphocytes and significant decreases in alveolar epithelial and endothelial cells. Neutrophil populations proved stable overall although several interferon-responding subsets demonstrated expansion. Spatial analysis revealed immune cell interactions occur prior to microscopically appreciable tissue injury.
    Interpretation: The immunopathogenesis of severe DAD in COVID-19 lung disease is characterised by sustained increases in MnPs and lymphocytes with key interactions occurring even prior to lung injury is established.
    Funding: UK Research and Innovation/Medical Research Council through the UK Coronavirus Immunology Consortium, Barbour Foundation, General Sir John Monash Foundation, Newcastle University, JGW Patterson Foundation, Wellcome Trust.
    Mesh-Begriff(e) Humans ; Young Adult ; Adult ; Middle Aged ; Aged ; Aged, 80 and over ; COVID-19/pathology ; Lung Injury/pathology ; Endothelial Cells ; SARS-CoV-2 ; Lung/pathology
    Sprache Englisch
    Erscheinungsdatum 2023-12-23
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2023.104945
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Interferon-γ-Producing CD4

    Romano, Audrey / Brown, Najmeeyah / Ashwin, Helen / Doehl, Johannes S P / Hamp, Jonathan / Osman, Mohamed / Dey, Nidhi / Rani, Gulab Fatima / Ferreira, Tiago Rodrigues / Kaye, Paul M

    Frontiers in immunology

    2021  Band 12, Seite(n) 700501

    Abstract: ... ...

    Abstract Ly6C
    Mesh-Begriff(e) Animals ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation/immunology ; Disease Models, Animal ; Interferon-gamma/immunology ; Leishmaniasis, Visceral/immunology ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology
    Chemische Substanzen Interferon-gamma (82115-62-6)
    Sprache Englisch
    Erscheinungsdatum 2021-09-07
    Erscheinungsland Switzerland
    Dokumenttyp 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.2021.700501
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  10. Artikel ; Online: TNF signalling drives expansion of bone marrow CD4+ T cells responsible for HSC exhaustion in experimental visceral leishmaniasis.

    Pinto, Ana Isabel / Brown, Najmeeyah / Preham, Olivier / Doehl, Johannes S P / Ashwin, Helen / Kaye, Paul M

    PLoS pathogens

    2017  Band 13, Heft 7, Seite(n) e1006465

    Abstract: Visceral leishmaniasis is associated with significant changes in hematological function but the mechanisms underlying these changes are largely unknown. In contrast to naïve mice, where most long-term hematopoietic stem cells (LT-HSCs; LSK CD150+ CD34- ... ...

    Abstract Visceral leishmaniasis is associated with significant changes in hematological function but the mechanisms underlying these changes are largely unknown. In contrast to naïve mice, where most long-term hematopoietic stem cells (LT-HSCs; LSK CD150+ CD34- CD48- cells) in bone marrow (BM) are quiescent, we found that during Leishmania donovani infection most LT-HSCs had entered cell cycle. Loss of quiescence correlated with a reduced self-renewal capacity and functional exhaustion, as measured by serial transfer. Quiescent LT-HSCs were maintained in infected RAG2 KO mice, but lost following adoptive transfer of IFNγ-sufficient but not IFNγ-deficient CD4+ T cells. Using mixed BM chimeras, we established that IFNγ and TNF signalling pathways converge at the level of CD4+ T cells. Critically, intrinsic TNF signalling is required for the expansion and/or differentiation of pathogenic IFNγ+CD4+ T cells that promote the irreversible loss of BM function. These findings provide new insights into the pathogenic potential of CD4+ T cells that target hematopoietic function in leishmaniasis and perhaps other infectious diseases where TNF expression and BM dysfunction also occur simultaneously.
    Mesh-Begriff(e) Animals ; Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; CD4-Positive T-Lymphocytes/cytology ; Cell Cycle ; Cell Proliferation ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Humans ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Leishmania donovani/physiology ; Leishmaniasis, Visceral/metabolism ; Leishmaniasis, Visceral/parasitology ; Leishmaniasis, Visceral/physiopathology ; Mice ; Mice, Inbred C57BL ; Signal Transduction ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
    Chemische Substanzen Tumor Necrosis Factor-alpha ; Interferon-gamma (82115-62-6)
    Sprache Englisch
    Erscheinungsdatum 2017-07-03
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7374
    ISSN (online) 1553-7374
    ISSN 1553-7374
    DOI 10.1371/journal.ppat.1006465
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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