• Sergio Scrimini, Jaume Pons, Alvar Agustí, Joan B Soriano, Borja G Cosio, Juan A Torrecilla, Belén Núñez, Rocío Córdova, Amanda Iglesias, Andreas Jahn, Catalina Crespi, and Jaume Sauleda.
• Fundación Investigación Sanitaria Illes Balears (FISIB), Hospital Universitari Son Espases, Palma de Mallorca, Spain; Centro de investigación biomédica en red de enfermedades respiratorias (CIBERES), Mallorca, Spain.
• Respir Med. 2013 Dec 1;107(12):1895-903.

BackgroundChronic obstructive pulmonary disease (COPD) is characterized by an enhanced and persistent innate and acquired immune response to tobacco smoking. Myeloid-derived suppressor cells (MDSCs) modulate T-cell responses by down-modulating the T cell receptor ζ chain (TCR ζ) through the catabolism of l-arginine. The effects of smoking on MDSCs and their potential participation in COPD immunopathogenesis have not been explored so far.MethodsTo investigate it, we compared the level of circulating Lineage-/HLA-DR-/CD33+/CD11b+ MDSCs, the serum concentration of arginase I (ARG I) and the expression of peripheral T-cell receptor ζ chain (TCR ζ) in never smokers, smokers with normal spirometry and COPD patients. Flow cytometry was used to quantify circulating MDSCs and TCR ζ expression. Serum ARG I levels were determined by ELISA.ResultsThe main findings of this study were that: (1) current smoking upregulates and activates circulating MDSCs both in smoker controls and COPD patients; and, (2) at variance with the smokers with normal spirometry, in patients with COPD this effect persists after quitting smoking and is accompanied by a significant and specific down-regulation of the TCR ζ chain expression in circulating T lymphocytes.ConclusionSmoking modulates circulating MDSCs. Their regulation appears altered in patients with COPD.Copyright © 2013 Elsevier Ltd. All rights reserved.

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