ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026
Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 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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Abstract
Intracerebral hemorrhage (ICH) is a devastating subtype of stroke, with a 5-year mortality of up to 70 %. Disease-modifying treatments to improve neurological outcomes in ICH survivors represent a critical unmet need. Neuroinflammation contributes significantly to ongoing secondary brain injury and long-term morbidity in ICH. We and others have shown that B cells are potent modulators of the inflammatory response, capable of acquiring a regulatory phenotype within injured microenvironments. Here, we investigated the effects of a single intraparenchymal application of mature naïve splenic B lymphocytes in a murine model of collagenase-induced ICH. In vivo tracking of luciferase-expressing B cells showed that the exogenous cells remained localized at the delivery site for up to 2 weeks. Delayed intraparenchymal B cell application at 24 h post-ICH was associated with acute neuroprotection of motor function in wire grip and rotarod assays and significant cognitive neuroprotection at 30 days post-injury in a Y maze paradigm. B cell administration was associated with reduced inflammasome activation at the injury site, diminished infiltration of CD8
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