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Impaired Function of Innate T Lymphocytes and NK Cells in the Acute Phase of Ischemic Stroke.

Authors :
Peterfalvi, Agnes
Molnar, Tihamer
Banati, Miklos
Pusch, Gabriella
Miko, Eva
Bogar, Lajos
Pal, Jozsef
Szereday, Laszlo
Illes, Zsolt
Source :
Cerebrovascular Diseases; Nov2009, Vol. 28 Issue 5, p490-498, 9p, 3 Charts, 4 Graphs
Publication Year :
2009

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-γ (IFN-γ) expression of Vδ2 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 Vδ2, NKT-like and NK cells were constant, and similar to percentages in healthy subjects. In contrast, proinflammatory intracellularIFN-γ expression by Vδ2 T cells, NKT-like cells and NK cells and IFN-γ 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 Vδ2 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-γ and perforin expression by Vδ2 T cells correlated with clinical improvement indicated by decreases in NIHSS scores. Conclusions: Pro-inflammatory and cytotoxic responses of NK, NKT-like and Vδ2 T cells become acutely deficient in ischemic stroke, which may contribute to an increased susceptibility to infections. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10159770
Volume :
28
Issue :
5
Database :
Complementary Index
Journal :
Cerebrovascular Diseases
Publication Type :
Academic Journal
Accession number :
44868917
Full Text :
https://doi.org/10.1159/000236527