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: In a cross-sectional design, we enrolled 148 patients with ischemic stroke and 30 age- and sex-matched healthy controls. Serum concentrations of IL-2 and IL-10 were quantified using ELISA, and TF gene expression in PBMCs was evaluated by real-time PCR. Stroke severity was assessed using the NIH Stroke Scale (NIHSS), and correlations with clinical variables were analyzed. 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 exhibited significantly reduced levels of IL-2 and IL-10 (p 0.001), and markedly increased TF removedp 0.001), compared to both mild stroke and control groups. TF levels demonstrated strong diagnostic accuracy for distinguishing stroke severity (AUC = 0.960, p 0.0001). IL-2 and TF were inversely correlated in severe cases (p = 0.036). However, none of the biomarkers independently predicted survival outcomes. 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 findings indicate a dysregulated immune-coagulation axis in severe ischemic stroke. Reduced IL-2 and IL-10 levels may reflect impaired regulatory T-cell activity and anti-inflammatory control, leading to monocyte activation and increased TF expression. This interplay likely exacerbates thromboinflammatory cascades, contributing to greater neurological damage. These alterations, while not predictive of survival, provide mechanistic insights into stroke pathophysiology and open avenues for targeted immunomodulatory therapy. 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.
Mohammadian et al. (Thu,) studied this question.
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