Review highlights immunological biomarkers' role in ischemic stroke outcomes, suggesting they can guide treatment and improve prognosis.
Ischemic stroke triggers a dynamic immune response that influences both acute damage and long-term recovery. This review synthesizes a decade of evidence on immunolog-ical and inflammatory biomarkers in ischemic stroke, emphasizing their prognostic and therapeutic significance. Following ischemic insult, pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, tumour necrosis factor-α (TNF-α), and chemokines like IL-8 rapidly rise, promoting blood-brain barrier disruption, leukocyte infiltration, and neu-ronal death. Conversely, anti-inflammatory mediators such as IL-10 and TGF-β facilitate repair, neurogenesis, and immune regulation in later phases. The balance between these pathways determines outcomes and is reflected in circulating biomarkers. Composite hematological indices including neutrophil-to-lymphocyte ratio (NLR), plate-let-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) offer accessible and cost-effective prognostic tools. Several biomarkers correlate with infarct size, neurological deterioration, and mortality, and may predict complications like hemorrhagic transformation or infection. Therapeutic strategies targeting cytokines, especially IL-1 and IL-6, have shown promise in modulating inflammation and im-proving outcomes. Future directions include personalized immune profiling, real-time cytokine monitoring, and combining immunotherapy with neurorestorative approach-es. By integrating immune biomarkers into stroke care, clinicians may enhance risk stratification, optimize treatment timing, and identify candidates for novel interven-tions. This review underscores inflammation’s dual role and evolving therapeutic and prognostic relevance in ischemic stroke.
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Iordache et al. (2025) studied this question.
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