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    An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD

    246942.pdf (788.0Kb)
    Access Status
    Open access
    Authors
    Tan, D.
    Ong, N.
    Zimmermann, M.
    Price, Patricia
    Moodley, Y.
    Date
    2016
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Tan, D. and Ong, N. and Zimmermann, M. and Price, P. and Moodley, Y. 2016. An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD. Human Immunology. 77 (10): pp. 916-920.
    Source Title
    Human Immunology
    DOI
    10.1016/j.humimm.2016.07.007
    ISSN
    0198-8859
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/23727
    Collection
    • Curtin Research Publications
    Abstract

    Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are characterized by increased pulmonary and systemic inflammation and commonly caused by bacterial and/or viral infection. Little is known about the T-cell dysregulation in AECOPD that promotes these outcomes. CD39 is an ectonucleotidase able to hydrolyse adenosine triphosphate to create adenosine that may inhibit T-cell responses in patients with AECOPD. Here T-cell expression of CD39 measured by flow cytometry was higher in AECOPD patients than stable COPD patients or healthy controls. Higher expression of CD39 was associated with higher levels of plasma soluble tumor necrosis factor receptor but lower interferon-γ (IFNγ) levels in supernatants from staphylococcal enterotoxin-B stimulated peripheral blood mononuclear cells. This links increased expression of CD39 with systemic inflammation and impaired T-cell responses (e.g. IFNγ). The blockade of CD39 pathways may be a novel approach to the control of AECOPD, reducing the dependency on antibiotics.

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