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

Dino Tan, N.E. Ong, M. Zimmermann, P. Price, Yuben Moodley

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

© 2016 American Society for Histocompatibility and ImmunogeneticsAcute 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-? (IFN?) 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. IFN?). The blockade of CD39 pathways may be a novel approach to the control of AECOPD, reducing the dependency on antibiotics.
Original languageEnglish
Pages (from-to)916-920
JournalHuman Immunology
Volume77
Issue number10
DOIs
Publication statusPublished - 2016

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Chronic Obstructive Pulmonary Disease
T-Lymphocytes
Histocompatibility
Tumor Necrosis Factor Receptors
Virus Diseases
Bacterial Infections
Adenosine
Interferons
Blood Cells
Pneumonia
Flow Cytometry
Adenosine Triphosphate
Anti-Bacterial Agents
Inflammation

Cite this

Tan, Dino ; Ong, N.E. ; Zimmermann, M. ; Price, P. ; Moodley, Yuben. / An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD. In: Human Immunology. 2016 ; Vol. 77, No. 10. pp. 916-920.
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An evaluation of CD39 as a novel immunoregulatory mechanism invoked by COPD. / Tan, Dino; Ong, N.E.; Zimmermann, M.; Price, P.; Moodley, Yuben.

In: Human Immunology, Vol. 77, No. 10, 2016, p. 916-920.

Research output: Contribution to journalArticle

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AU - Price, P.

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AB - © 2016 American Society for Histocompatibility and ImmunogeneticsAcute 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-? (IFN?) 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. IFN?). The blockade of CD39 pathways may be a novel approach to the control of AECOPD, reducing the dependency on antibiotics.

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