Cellular Physiology and Biochemistry · 2015 · 27 citations · 35 references
MedicineCardiologyImmunologyClinical ImmunologyImmunoregulationInflammationAcute Coronary SyndromesCardiovascular DiseaseCytokine BiologyCytokine RegulationIschemic Heart DiseaseMyeloid-derived Suppressor CellsCell Proliferation IndicesMonocytic Myeloid-derived Suppressor CellsMyeloid-derived Suppressor Cell CytokinesMyeloid-derived Suppressor Cell ExpansionMyeloid-derived Suppressor Cell FunctionMyeloid-derived Suppressor Cell ImmunosuppressionMyeloid-derived Suppressor Cell PhenotypeMyeloid-derived Suppressor Cell-mediated Suppression
AIM: The aim of this study was to explore whether the circulating frequency and function of myeloid-derived suppressor cells (MDSCs) are altered in patients with acute coronary syndrome (ACS). METHODS: The frequency of MDSCs in peripheral blood was determined by flow cytometry, and mRNA expression in purified MDSCs was analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR). The suppressive function of MDSCs isolated from different groups was also determined. The plasma levels of certain cytokines were determined using Bio-Plex Pro™ Human Cytokine Assays. RESULTS: The frequency of circulating CD14(+)HLA-DR(-/low) MDSCs; arginase-1 (Arg-1) expression; and plasma levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-33 were markedly increased in ACS patients compared to stable angina (SA) or control patients. Furthermore, MDSCs from ACS patients were more potent suppressors of T-cell proliferation and IFN-γ production than those from the SA or control groups at ratios of 1:4 and 1:2; this effect was partially mediated by Arg-1. In addition, the frequency of MDSCs was positively correlated with plasma levels of IL-6, IL-33, and TNF-α. CONCLUSIONS: We observed an increased frequency and suppressive function of MDSCs in ACS patients, a result that may provide insights into the mechanisms involved in ACS.
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C. Marcela Díaz‐Montero, Mohamed L. Salem, Michael I. Nishimura et al. · Cancer Immunology Immunotherapy · 2008 · 1.2K citations
Medicine, Cancer Biology, Oncology +17