{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T22:32:42Z","timestamp":1788820362976,"version":"build-2803163510"},"reference-count":156,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T00:00:00Z","timestamp":1768176000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Ischemic stroke (IS) is a leading cause of death and long-term disability globally, and the efficacy of current reperfusion therapies is limited, highlighting a significant unmet clinical need. This review reconceptualizes IS not as a mere focal brain injury but as a systemic disease driven by the catastrophic collapse of the Neuroimmune Regulatory Circuitry. This sophisticated network, normally responsible for maintaining homeostasis, undergoes a multi-level failure after stroke, beginning with pathological sensory input and culminating in a dysregulated efferent response characterized by sustained sympathetic hyperactivity and Hypothalamic-Pituitary-Adrenal (HPA) axis dysfunction. These aberrant neural commands pathologically alter the phenotype and function of peripheral immune cells, leading to a profound immune imbalance: emergency hematopoiesis generates primed, pro-inflammatory myeloid cells, while the\u00a0lymphoid lineage suffers massive depletion through apoptosis and\u00a0sequestration, causing severe lymphopenia. This framework unifies seemingly disparate post-stroke complications\u2014such as Stroke-Induced Immunosuppression (SIIS) and subsequent infections, long-term cardiovascular events fueled by chronic inflammation, and cognitive decline driven by persistent neuroinflammation\u2014as predictable outcomes of this circuitry failure. Consequently, this review argues for a paradigm shift away from single-target therapies towards an \u201cintegrative and sequential\u201d approach to treatment. Future strategies should aim to recalibrate this entire circuit, leveraging biomarkers to overcome patient heterogeneity and applying temporally-dependent interventions that inhibit acute injury while promoting chronic repair. This provides a more rational foundation for developing effective neuroprotective and restorative therapies for stroke patients.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1702245","type":"journal-article","created":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T08:12:37Z","timestamp":1768205557000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["From disruption to remodeling: the evolution and therapeutic prospects of Neuroimmune Regulatory Circuitry after ischemic 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