title: Phenotypic and functional alterations on inflammatory peripheral blood cells after acute myocardial infarction.
abstract: The frequency and function of T cells, monocytes, and dendritic cell subsets were investigated in 12 patients after acute myocardial infarction (AMI)-(T0), 1 month after the episode (T1), and in 12 healthy individuals (HG). The cell characterization and the functional studies were performed by flow cytometry and by RT-PCR, after cell sorting. The most important findings at T0 moment, when compared with T1 and HG, were: a decrease in the frequency of IL-2-producing T cells; a lower frequency of TNF-α- and IL-6-producing monocytes, myeloid dendritic cells, and CD14(-/low)CD16(+)DCs; and a lower TNF-α mRNA expression, after sorting these cells. Moreover, the regulatory function of Treg cells, at T0 moment, was upregulated, based on the FoxP3, CTLA-4, and TGF-β mRNA expression increase. The majority of these phenotypic and functional alterations disappeared at T1. Our data demonstrate that AMI induces a significant change in the immune system homeostasis.
authors.affiliation: Histocompatibility Centre of Coimbra, Edifício São Jerónimo, 4° Piso, Praceta Mota Pinto, 3001-301 Coimbra, Portugal.
authors.forename: Tiago
authors.initials: T
authors.lastname: Carvalheiro
authors.forename: Isabel
authors.initials: I
authors.lastname: Velada
authors.forename: Ana
authors.initials: A
authors.lastname: Valado
authors.forename: Fernando
authors.initials: F
authors.lastname: Mendes
authors.forename: António
authors.initials: A
authors.lastname: Martinho
authors.forename: Natália
authors.initials: N
authors.lastname: António
authors.forename: Lino
authors.initials: L
authors.lastname: Gonçalves
authors.forename: Luís
authors.initials: L
authors.lastname: Providência
authors.forename: Maria Luísa
authors.initials: ML
authors.lastname: Pais
authors.forename: Artur
authors.initials: A
authors.lastname: Paiva
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002469:Cell Separation; D003713:Dendritic Cells / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins / Q000097:blood; D006801:Humans; D016130:Immunophenotyping; D007249:Inflammation / Q000097:blood / Q000235:genetics / Q000276:immunology*; D018836:Inflammation Mediators / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics / Q000276:immunology*; D010641:Phenotype; D011174:Portugal; D011446:Prospective Studies; D012333:RNA, Messenger / Q000097:blood; D060888:Real-Time Polymerase Chain Reaction; D017452:Receptors, IgG / Q000097:blood; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
chemical_list: D015415:Biomarkers; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; C508594:IL2 protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D007376:Interleukin-2; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D017452:Receptors, IgG; D014409:Tumor Necrosis Factor-alpha