ArticleJournal of neuroinflammation2023
B cell treatment promotes a neuroprotective microenvironment after traumatic brain injury through reciprocal immunomodulation with infiltrating peripheral myeloid cells.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Bridging the gap: neuroinflammation and the dawn of precision medicine in amyotrophic lateral sclerosis.Translational neurodegeneration · 2026Review
- Compartmentalized B cell-microglia crosstalk drives ischemic white matter demyelination.Nature communications · 2026Article
- Innovative Biomaterials for Modulating Neuroinflammation and Promoting Repair After Traumatic Brain Injury.Pharmaceutics · 2026Review
- Regulatory B cells in the central nervous system: From immune regulation to neuroprotection.Neuroprotection (Chichester, England) · 2026Review
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Neuroimmune Mechanisms in Traumatic Brain Injury and Cancer: Parallel Courses or Existence in Different Orbits.Biomedicines · 2026Review
- Extracellular vesicle-mediated immunomodulation and targeted delivery: breakthroughs and challenges in rheumatoid arthritis therapy.Frontiers in immunology · 2026Review
- 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
- Sex differences in neurobehavior and the adult hippocampal neurogenic niche: influence of traumatic brain injury and CLIP antagonism.Frontiers in behavioral neuroscience · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- GsMTx4 Mitigates Neuroinflammation and Promotes Functional Recovery by Maintaining Microenvironmental Homeostasis During the Acute Phase After Traumatic Brain Injury in Mice.Neurochemical research · 2025Article
- Reticuline modulates astrocyte and microglial responses to enhance prognosis after traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Interleukin-35 impairs human NK cell effector functions and induces their ILC1-like conversion with tissue residency features.Nature communications · 2025Article
- B cells in non-lymphoid tissues.Nature reviews. Immunology · 2025Review
- The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models.Frontiers in neurology · 2025Review
- SIV-specific antibodies protect against inflammasome-driven encephalitis in untreated macaques.Cell reports · 2024Article
- Traumatic brain injury alters the effects of class II invariant peptide (CLIP) antagonism on chronic meningeal CLIP + B cells, neuropathology, and neurobehavioral impairment in 5xFAD mice.Journal of neuroinflammation · 2024Article
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- Elucidating the neuroimmunology of traumatic brain injury: methodological approaches to unravel intercellular communication and function.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) remains a major cause of death and severe disability worldwide. We found previously that treatment with exogenous naïve B cells was associated with structural and functional neuroprotection after TBI. Here, we used a mouse model of unilateral controlled cortical contusion TBI to investigate cellular mechanisms of immunomodulation associated with intraparenchymal delivery of mature naïve B lymphocytes at the time of injury. Exogenous B cells showed a complex time-dependent response in the injury microenvironment, including significantly increased expression of IL-10, IL-35, and TGFβ, but also IL-2, IL-6, and TNFα. After 10 days in situ, B cell subsets expressing IL-10 or TGFβ dominated. Immune infiltration into the injury predominantly comprised myeloid cells, and B cell treatment did not alter overall numbers of infiltrating cells. In the presence of B cells, significantly more infiltrating myeloid cells produced IL-10, TGFβ, and IL-35, and fewer produced TNFα, interferon-γ and IL-6 as compared to controls, up to 2 months post-TBI. B cell treatment significantly increased the proportion of CD206
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.