ArticleCell death discovery2026
Antler stem cells effectively alleviate the symptoms of cerebral ischemic injury via immunomodulation of the spleen.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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14 authors.
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Abstract
Ischemic stroke is a major cause of disability and mortality worldwide. Increasing evidence indicates that peripheral immune responses contribute to secondary brain injury after stroke. The impact of the splenic response on brain injury has been well documented in animal models. This phenomenon remains poorly defined in the clinical situation. Through a retrospective analysis of 76 patients with acute anterior circulation large-vessel occlusion, we provide novel evidence that post-stroke spleen volume reduction is an outstanding risk factor for cerebral edema expansion, an association partially explained by a concomitant decrease in peripheral lymphocytes. Previous studies have shown that bone marrow-derived mesenchymal stem cells (BMSCs) improve stroke outcomes through immunomodulation peripherally. Nonetheless, efforts to identify more potent MSCs have never ceased. Antler stem cells, known for their potent regenerative and anti-inflammatory properties, represent promising candidates for stroke treatment. Using the transient middle cerebral artery occlusion (tMCAO) model rats, we found that intravenous administration of antler reserve mesenchymal cells (aRMCs, one type of antler stem cells) significantly improved motor function and reduced both cerebral edema and infarct volume, effects that were superior to those observed with BMSC treatment. Notably, these beneficial effects of aRMCs were attenuated in the splenectomized animals. Compared with the model and BMSC groups, the spleens of aRMC-treated rats exhibited increased weight, restored T cell populations, reduced lymphocyte activity, and downregulated expression of T cell migration-related genes. Additionally, these rats displayed decreased T cell infiltration into the cerebral infarct region. Mechanistically, the inhibitory effect of aRMCs on tMCAO-induced splenic T-cell migration is highly likely to be achieved via downregulation of CCR5 expression. These findings demonstrate a causal link between the degree of splenic contraction and the severity of brain edema, suggest spleen-to-brain T-cell migration as a therapeutic target, and position aRMCs as a promising and novel stem cell type for post-stroke neuroprotection with superior efficacy over BMSCs.
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