ArticleNeurobiology of disease2025
B cells upregulate NMDARs, respond to extracellular glutamate, and express mature BDNF to protect the brain from ischemic injury.
Article in Neurobiology of disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Integrated B and T Cell Repertoire Analysis Reveals Organized but Heterogeneous Adaptive Immunity in Chronic Experimental Stroke.Research square · 2026Article
- Shared transcriptomic signatures in perilesional and contralesional cortex after ischemic stroke.Journal of neuroinflammation · 2026Article
- Age-associated B cells (ABCs) develop from a CNS-localized progenitor pool into a pro-inflammatory phenotype after stroke.bioRxiv : the preprint server for biology · 2026Article
- Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026Article
- Peripheral B cell populations tune spontaneous neuronal activity in the uninjured hippocampus after stroke.bioRxiv : the preprint server for biology · 2026Article
- Shared Transcriptomic Signatures in Perilesional and Contralesional Cortex.bioRxiv : the preprint server for biology · 2026Article
- Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Following stroke, B cells enter brain regions outside of the ischemic injury to mediate functional recovery. Although B cells produce neurotrophins that support remote plasticity, including brain-derived neurotrophic factor (BDNF), it remains unclear which signal(s) activate B cells in the absence of infarct-localized pro-inflammatory cues. Activation of N-methyl-d-aspartate (NMDA)-type receptor (NMDAR) subunits on neurons can upregulate mature BDNF (mBDNF) production from a pro-BDNF precursor, but whether this occurs in B cells is unknown. We identified GluN2A and GluN2B NMDAR subunits on B cells that respond to glutamate and mediate nearly half of the glutamate-induced Ca
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