The proportion and function of peripheral myeloid-derived suppressor cells do not correlate with systemic inflammation in chronic obstructive pulmonary disease

Dino Tan, Sonia Fernández, Patricia Price, Yuben Moodley

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Abstract

Myeloid-derived suppressor cells (MDSC) have been implicated in the regulation of chronic inflammation. Chronic obstructive pulmonary disease (COPD) involves persistent inflammation, but the role of MDSC has not been explored. Here, proportions of MDSC (CD14-HLA-DR-CD33+CD11b+ cells) were quantified in peripheral blood mononuclear cells (PBMC) isolated from patients with 'stable' COPD (n=12), smokers with no evidence of COPD (n=11) and healthy non-smokers (n=11). The proportions of MDSC were similar in all groups. MDSC function was assessed by comparing T-cell and cytokine responses of whole and MDSC-depleted PBMC stimulated with Staphylococcus enterotoxin-B (SEB). Depletion of MDSC did not enhance CD4+ or CD8+ T-cell activation and proliferation, or alter IFNγ and IL-17 production in response to SEB. However production of TGFβ decreased after depletion of MDSC, so MDSC may be a source of this cytokine. In conclusion, COPD was not associated with perturbations in the proportion or function of MDSC in peripheral blood. © 2013 American Society for Histocompatibility and Immunogenetics.
Original languageEnglish
Pages (from-to)5-9
JournalHuman Immunology
Volume75
Issue number1
DOIs
Publication statusPublished - 2014

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Chronic Obstructive Pulmonary Disease
Inflammation
Blood Cells
Myeloid-Derived Suppressor Cells
Cytokines
T-Lymphocytes
Interleukin-17
HLA-DR Antigens
Cell Proliferation

Cite this

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title = "The proportion and function of peripheral myeloid-derived suppressor cells do not correlate with systemic inflammation in chronic obstructive pulmonary disease",
abstract = "Myeloid-derived suppressor cells (MDSC) have been implicated in the regulation of chronic inflammation. Chronic obstructive pulmonary disease (COPD) involves persistent inflammation, but the role of MDSC has not been explored. Here, proportions of MDSC (CD14-HLA-DR-CD33+CD11b+ cells) were quantified in peripheral blood mononuclear cells (PBMC) isolated from patients with 'stable' COPD (n=12), smokers with no evidence of COPD (n=11) and healthy non-smokers (n=11). The proportions of MDSC were similar in all groups. MDSC function was assessed by comparing T-cell and cytokine responses of whole and MDSC-depleted PBMC stimulated with Staphylococcus enterotoxin-B (SEB). Depletion of MDSC did not enhance CD4+ or CD8+ T-cell activation and proliferation, or alter IFNγ and IL-17 production in response to SEB. However production of TGFβ decreased after depletion of MDSC, so MDSC may be a source of this cytokine. In conclusion, COPD was not associated with perturbations in the proportion or function of MDSC in peripheral blood. {\circledC} 2013 American Society for Histocompatibility and Immunogenetics.",
author = "Dino Tan and Sonia Fern{\'a}ndez and Patricia Price and Yuben Moodley",
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TY - JOUR

T1 - The proportion and function of peripheral myeloid-derived suppressor cells do not correlate with systemic inflammation in chronic obstructive pulmonary disease

AU - Tan, Dino

AU - Fernández, Sonia

AU - Price, Patricia

AU - Moodley, Yuben

PY - 2014

Y1 - 2014

N2 - Myeloid-derived suppressor cells (MDSC) have been implicated in the regulation of chronic inflammation. Chronic obstructive pulmonary disease (COPD) involves persistent inflammation, but the role of MDSC has not been explored. Here, proportions of MDSC (CD14-HLA-DR-CD33+CD11b+ cells) were quantified in peripheral blood mononuclear cells (PBMC) isolated from patients with 'stable' COPD (n=12), smokers with no evidence of COPD (n=11) and healthy non-smokers (n=11). The proportions of MDSC were similar in all groups. MDSC function was assessed by comparing T-cell and cytokine responses of whole and MDSC-depleted PBMC stimulated with Staphylococcus enterotoxin-B (SEB). Depletion of MDSC did not enhance CD4+ or CD8+ T-cell activation and proliferation, or alter IFNγ and IL-17 production in response to SEB. However production of TGFβ decreased after depletion of MDSC, so MDSC may be a source of this cytokine. In conclusion, COPD was not associated with perturbations in the proportion or function of MDSC in peripheral blood. © 2013 American Society for Histocompatibility and Immunogenetics.

AB - Myeloid-derived suppressor cells (MDSC) have been implicated in the regulation of chronic inflammation. Chronic obstructive pulmonary disease (COPD) involves persistent inflammation, but the role of MDSC has not been explored. Here, proportions of MDSC (CD14-HLA-DR-CD33+CD11b+ cells) were quantified in peripheral blood mononuclear cells (PBMC) isolated from patients with 'stable' COPD (n=12), smokers with no evidence of COPD (n=11) and healthy non-smokers (n=11). The proportions of MDSC were similar in all groups. MDSC function was assessed by comparing T-cell and cytokine responses of whole and MDSC-depleted PBMC stimulated with Staphylococcus enterotoxin-B (SEB). Depletion of MDSC did not enhance CD4+ or CD8+ T-cell activation and proliferation, or alter IFNγ and IL-17 production in response to SEB. However production of TGFβ decreased after depletion of MDSC, so MDSC may be a source of this cytokine. In conclusion, COPD was not associated with perturbations in the proportion or function of MDSC in peripheral blood. © 2013 American Society for Histocompatibility and Immunogenetics.

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