title: Impaired function of innate T lymphocytes and NK cells in the acute phase of ischemic stroke.
abstract: BACKGROUND
  Functional alterations of innate lymphocytes, which can mount rapid immune responses and shape subsequent T cell reactions, were examined in the acute phase of ischemic stroke.
  
  
  METHODS
  Frequencies, intracellular perforin and interferon-gamma (IFN-gamma) expression of Vdelta2 T cells, CD3+ CD56+ natural killer T (NKT)-like and NK cells were examined in the peripheral blood of 20 healthy controls and 28 patients within 6 h of the onset of acute ischemic stroke and after 72 h by flow cytometry. Cytokine production of isolated NKT-like and NK cells following in vitro activation was measured by cytometric bead array. NK cytotoxicity was examined in the peripheral blood mononuclear cells.
  
  
  RESULTS
  Percentages of Vdelta2, NKT-like and NK cells were constant, and similar to percentages in healthy subjects. In contrast, proinflammatory intracellularIFN-gamma expression by Vdelta2 T cells, NKT-like cells and NK cells and IFN-gamma production by isolated NK cells in culture was low at 6 h and reached the level of healthy subjects by 72 h after stroke. Production of anti-inflammatory cytokines was unaltered. Intracellular perforin expression by Vdelta2 T cells, NKT-like cells and NK cells, and NK cytotoxicity was low at 6 h, and reached the level of healthy subjects by 72 h. Increases in IFN-gamma and perforin expression by Vdelta2 T cells correlated with clinical improvement indicated by decreases in NIHSS scores.
  
  
  CONCLUSIONS
  Pro-inflammatory and cytotoxic responses of NK, NKT-like and Vdelta2 T cells become acutely deficient in ischemic stroke, which may contribute to an increased susceptibility to infections.
authors.affiliation: Department of Neurology, University of Pécs, Pécs, Hungary.
authors.forename: Agnes
authors.initials: A
authors.lastname: Peterfalvi
authors.forename: Tihamer
authors.initials: T
authors.lastname: Molnar
authors.forename: Miklos
authors.initials: M
authors.lastname: Banati
authors.forename: Gabriella
authors.initials: G
authors.lastname: Pusch
authors.forename: Eva
authors.initials: E
authors.lastname: Miko
authors.forename: Lajos
authors.initials: L
authors.lastname: Bogar
authors.forename: Jozsef
authors.initials: J
authors.lastname: Pal
authors.forename: Laszlo
authors.initials: L
authors.lastname: Szereday
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Illes
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002545:Brain Ischemia / Q000276:immunology*; D002469:Cell Separation; D016207:Cytokines / Q000096:biosynthesis; D053222:Fas Ligand Protein / Q000096:biosynthesis; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007371:Interferon-gamma / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology* / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D020521:Stroke / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology
chemical_list: D016207:Cytokines; D053222:Fas Ligand Protein; D007371:Interferon-gamma