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Impaired Function of Innate T Lymphocytes and NK Cells in the Acute Phase of Ischemic Stroke.
- 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]
- Subjects :
- T cells
CEREBROVASCULAR disease
CELLULAR immunity
CYTOKINES
CYTOMETRY
INFLAMMATION
Subjects
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