Cytotoxic function of CD8+ T lymphocytes isolated from patients with acute severe cerebral infarction: An assessment of stroke-induced immunosuppression

Abstract

Background: There is increasing evidence on complex interaction between the nervous and immune systems in patients with cerebral infarction. This study was conducted to evaluate cytotoxic function of CD8+ T lymphocytes isolated from patients with acute severe cerebral infarction. In order to determine role of immune system in stroke, peripheral blood mononuclear cells (PBMCs) were taken and cytotoxic function of CD8+ T lymphocytes were induced by virus peptides and cells were analyzed on a four-color flow cytometer. Expression of CD107a, intracellular expression of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α), and cell proliferation assay were analyzed by using carboxyl fluorescein diacetate succinimidyl ester (CFSE).Results: A total of 30 patients with cerebral infarction and 30 healthy volunteers with an average age 57 (range, 49 to 71) years, were evaluated. The PBMCs were separated from blood samples of both, patients with cerebral infarction 6 hours after onset of stroke and healthy volunteers. After stimulation with virus peptides, CD107a expression and intracellular production of IFN-γ and TNF-α was decreased in patients with cerebral infarction as compared to healthy volunteers (p < 0.01). Degranulation analysis reported decreased expression of CD107a + in patient group as compared to healthy group, p <0.01. A mild decrease in intracellular expression of IFN-γ and TNF-α was also shown in patients without stimulation of virus peptides (p < 0.05). However, proliferation of CD8+ T lymphocytes in patients with acute severe cerebral infarction was not decreased.Conclusions: The study results indicated that cytotoxic function of CD8+ T lymphocytes were suppressed in patients with acute severe cerebral infarction. This could possibly be associated with complicated infectious diseases and neuroprotective mechanism. © 2013 Li et al.; licensee BioMed Central Ltd.