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Updated: Apr 4, 2026
Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
Decreased Anti-inflammatory IL-2 and IL-10 and Increased Mononuclear Cell Tissue Factor Correlate with Stroke
Kiana Mohammadian1,2, Tahereh Kalantari2,3, Rasoul Ebrahimi1,2
1Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Introduction:
Inflammatory and coagulation pathways are crucial in the pathogenesis and clinical progression of ischemic stroke. The objective of this study was to evaluate serum concentrations of interleukin-2 (IL-2) and interleukin-10 (IL-10), as well as the gene expression of tissue factor (TF) in peripheral blood mononuclear cells (PBMCs), and to examine their correlations with stroke severity and clinical outcomes.
Materials And Methods:
We enrolled 148 patients with ischemic stroke and 30 healthy controls matched for age and sex in a cross-sectional design. We used ELISA to measure the levels of IL-2 and IL-10 in serum and real-time PCR to look at TF gene expression in PBMCs. The NIH Stroke Scale (NIHSS) was used to measure the severity of strokes, and the results were compared to clinical variables.
Results:
Patients with severe stroke showed significantly lower levels of IL-2 and IL-10 (p < 0.001), and TF expression in PBMCs was significantly higher in both mild and severe stroke groups compared to controls (p < 0.001). There was no statistically significant difference between the mild and severe groups (p = 0.213). In severe cases, IL-2 and TF were negatively correlated (p = 0.036). Nonetheless, none of the biomarkers independently forecasted survival outcomes.
Discussion:
The results show that the immune-coagulation axis is not working properly in severe ischemic stroke. Lower levels of IL-2 and IL-10 may indicate that regulatory T-cells aren't working properly and that anti-inflammatory control isn't working, which can cause monocytes to become active and TF levels to rise. This interaction probably makes thromboinflammatory cascades worse, which leads to more damage to the nervous system. These changes, even though they don't predict survival, give us a better understanding of how strokes work and open up new possibilities for targeted immunomodulatory therapy.
Conclusion:
The changes in IL-2, IL-10, and TF expression indicate a coordinated disruption of immune and thrombotic pathways in individuals with severe ischemic stroke. Although not prognostic of mortality, these biomarkers may indicate disease severity and represent potential targets for future therapeutic interventions. Longitudinal studies are necessary to validate their prognostic significance and investigate their incorporation into clinical decision-making algorithms for stroke.
