Immunomodulation of microglia/macrophages and neutrophils as immunotherapeutic targets in ischemic stroke: A narrative review

Abstract Ischemic stroke (IS) remains a critical global issue characterized by high mortality and morbidity rates, primarily caused by neuronal death and brain dysfunction resulting from vascular occlusion. In secondary injuries following IS, inflammation plays a vital role, leading to increased neuronal damage and a poorer prognosis in the early stages. However, inflammation serves a dual purpose in stroke pathophysiology, promoting tissue repair and healing, especially in the later stages of stroke. Mechanical thrombectomy and intravenous thrombolysis are the primary therapeutic choices for IS. However, their narrow therapeutic windows and increased bleeding risks remain problematic. Recent research highlights the therapeutic potential of regulating immune cells, focusing on microglia, macrophages, and neutrophils, due to their dual roles in IS. Current preclinical and clinical studies have shown that this strategy holds promise in the prevention and management of IS. The aim of this review to assess the evolving landscape of immune modulation as therapeutic avenue in ischemic stroke.