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Preparation of Myeloid Derived Suppressor Cells (MDSC) from Naive and Pancreatic Tumor-bearing Mice using Flow Cytometry and Automated Magnetic Activated Cell Sorting (AutoMACS)
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Preparation of Myeloid Derived Suppressor Cells (MDSC) from Naive and Pancreatic Tumor-bearing Mice using Flow Cytometry and Automated Magnetic Activated Cell Sorting (AutoMACS)

Published on: June 18, 2012

The proportion and function of peripheral myeloid-derived suppressor cells do not correlate with systemic

Dino B A Tan1, Sonia Fernandez2, Patricia Price2

  • 1Centre for Asthma, Allergy and Respiratory Research, The Lung Institute of Western Australia, The University of Western Australia, Nedlands, Australia; School of Medicine and Pharmacology, The University of Western Australia, Nedlands, Australia.

Human Immunology
|October 5, 2013
PubMed

Insights

Myeloid-derived suppressor cells (MDSC) proportions and function were similar in chronic obstructive pulmonary disease (COPD) patients and controls. MDSC depletion reduced TGFβ, suggesting a role in its production, but did not impact T-cell responses in COPD.

Area of Science:

  • Immunology
  • Pulmonology
  • Cell Biology

Background:

  • Myeloid-derived suppressor cells (MDSC) are key regulators of chronic inflammation.
  • Chronic obstructive pulmonary disease (COPD) is characterized by persistent inflammation.
  • The specific role of MDSC in COPD pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the proportion and function of MDSC in patients with stable COPD.
  • To compare MDSC levels and activity between COPD patients, smokers, and healthy individuals.
  • To elucidate the contribution of MDSC to immune dysregulation in COPD.

Main Methods:

  • Quantification of MDSC (CD14(-)HLA-DR(-)CD33(+)CD11b(+) cells) in peripheral blood mononuclear cells (PBMC).
  • Comparison of MDSC proportions in stable COPD patients (n=12), smokers (n=11), and healthy non-smokers (n=11).
  • Assessment of MDSC function via T-cell activation and cytokine production (IFNγ, IL-17, TGFβ) after Staphylococcus enterotoxin-B (SEB) stimulation, with and without MDSC depletion.

Main Results:

  • MDSC proportions were comparable across all study groups (COPD, smokers, healthy controls).
  • Depletion of MDSC did not alter CD4(+) or CD8(+) T-cell activation, proliferation, or IFNγ and IL-17 production.
  • A decrease in TGFβ production was observed after MDSC depletion, indicating MDSC as a potential source of this cytokine.

Conclusions:

  • COPD is not associated with altered proportions of peripheral blood MDSC.
  • MDSC function, in terms of T-cell activation and key cytokine production, is not significantly perturbed in stable COPD.
  • MDSC may contribute to TGFβ production, warranting further investigation in inflammatory lung diseases.

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