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

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 ectonucl...

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Main Authors: Tan, D., Ong, N., Zimmermann, M., Price, Patricia, Moodley, Y.
Format: Journal Article
Published: Elsevier Inc. 2016
Online Access:http://hdl.handle.net/20.500.11937/23727
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author Tan, D.
Ong, N.
Zimmermann, M.
Price, Patricia
Moodley, Y.
author_facet Tan, D.
Ong, N.
Zimmermann, M.
Price, Patricia
Moodley, Y.
author_sort Tan, D.
building Curtin Institutional Repository
collection Online Access
description 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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spelling curtin-20.500.11937-237272017-09-13T16:00:09Z An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD Tan, D. Ong, N. Zimmermann, M. Price, Patricia Moodley, Y. 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. 2016 Journal Article http://hdl.handle.net/20.500.11937/23727 10.1016/j.humimm.2016.07.007 Elsevier Inc. fulltext
spellingShingle Tan, D.
Ong, N.
Zimmermann, M.
Price, Patricia
Moodley, Y.
An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title_full An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title_fullStr An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title_full_unstemmed An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title_short An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD
title_sort evaluation of cd39 as a novel immunoregulatory mechanism invoked by copd
url http://hdl.handle.net/20.500.11937/23727