title: Enhanced expression of inflammatory cytokines and activation markers in T-cells from patients with chronic heart failure.
abstract: OBJECTIVE
  Increasing evidence supports a role for inflammation in chronic heart failure (CHF). However, the source and the mechanism for this immune activation are unknown. To address this issue we investigated the gene expression of cytokines and the surface expression of activity markers in T-cells and monocytes from CHF patients and healthy controls.
  
  
  METHODS
  Gene expression of cytokines was analysed by real-time RT-PCR and activation markers by flow cytometry in 14 CHF patients and nine healthy controls. Surface expression of activation markers for T-cells and monocytes were analysed by flow cytometry.
  
  
  RESULTS
  T-cells from CHF patients showed enhanced gene expression of chemokines, ligands in the tumor necrosis factor superfamily, as well as the inflammatory cytokines interferon-gamma and interleukin-18 with similar pattern in ischemic (n=5) and idiopathic cardiomyopathy (n=9). In contrast, no differences in cytokine gene expression were found comparing monocytes from CHF patients and controls. Moreover, T-cells from CHF patients had enhanced surface expression of the activation markers CD69 and CD25, while there was no upregulation of the monocyte activation marker CD32 in these patients.
  
  
  CONCLUSIONS
  T-cells may be a part of the inflammatory response during CHF independent of the etiology of the disorder. Intervention preventing unwanted T-cell activation could represent a new target in the treatment of CHF.
authors.affiliation: Research Institute for Internal Medicine, Rikshospitalet, University of Oslo, N-0027, Oslo, Norway. arne.yndestad@klinmed.uio.no
authors.forename: Arne
authors.initials: A
authors.lastname: Yndestad
authors.forename: Are M
authors.initials: AM
authors.lastname: Holm
authors.forename: Fredrik
authors.initials: F
authors.lastname: Müller
authors.forename: Svein
authors.initials: S
authors.lastname: Simonsen
authors.forename: Stig S
authors.initials: SS
authors.lastname: Frøland
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D002303:Cardiac Output, Low / Q000276:immunology*; D016022:Case-Control Studies; D002908:Chronic Disease; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D020382:Interleukin-18 / Q000276:immunology; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis; D015375:Receptors, Interleukin-2 / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D015415:Biomarkers; D016207:Cytokines; D007371:Interferon-gamma; D020382:Interleukin-18; D037181:Lectins, C-Type; D012333:RNA, Messenger; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D000099192:CD69 Antigens