ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2016
B-Cell Depletion Reduces the Maturation of Cerebral Cavernous Malformations in Murine Models.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Cerebral cavernous malformations: epidemiology, molecular pathogenesis, diagnosis and therapy.Molecular biomedicine · 2026Review
- CXCL13⁺ CD4⁺ T cells are associated with B-cell recruitment and lesion progression in cerebral cavernous malformations.Journal of neuroinflammation · 2026Article
- The Role of Immune Infiltration and Oxidative Stress in the Progression of Cerebral Cavernous Malformation.Brain and behavior · 2026Review
- FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity.Journal of virology · 2025Article
- Focused ultrasound augments the delivery and penetration of model therapeutics into cerebral cavernous malformations.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Persistent Activation of Endothelial Cells is Linked to Thrombosis and Inflammation in Cerebral Cavernous Malformation Disease.bioRxiv : the preprint server for biology · 2025Article
- Review
- Pharmacological blocking of neutrophil extracellular traps attenuates immunothrombosis and neuroinflammation in cerebral cavernous malformation.Nature cardiovascular research · 2024Article
- KRIT1 in vascular biology and beyond.Bioscience reports · 2024Review
- Behavioral impairments are linked to neuroinflammation in mice with Cerebral Cavernous Malformation disease.bioRxiv : the preprint server for biology · 2024Article
- Trial Readiness of Cavernous Malformations With Symptomatic Hemorrhage, Part II: Biomarkers and Trial Modeling.Stroke · 2024Article
- Inflammatory Mechanisms in a Neurovascular Disease: Cerebral Cavernous Malformation.Brain sciences · 2023Review
- Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformation Disease.Circulation research · 2022Article
- Dysregulated Hemostasis and Immunothrombosis in Cerebral Cavernous Malformations.International journal of molecular sciences · 2022Review
- Cerebral Cavernous Malformation Pathogenesis: Investigating Lesion Formation and Progression with Animal Models.International journal of molecular sciences · 2022Review
- Inflammation and neutrophil extracellular traps in cerebral cavernous malformation.Cellular and molecular life sciences : CMLS · 2022Article
- Article
- Elevated proportion of TLR2- and TLR4-expressing Th17-like cells and activated memory B cells was associated with clinical activity of cerebral cavernous malformations.Journal of neuroinflammation · 2022Article
- Cerebral Cavernous Malformation: Immune and Inflammatory Perspectives.Frontiers in immunology · 2022Review
- Cerebral Cavernous Malformation: From Mechanism to Therapy.Circulation research · 2021Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Cerebral cavernous malformations (CCMs) are relatively common vascular malformations, characterized by increased Rho kinase (ROCK) activity, vascular hyper-permeability and the presence of blood degradation products including non-heme iron. Previous studies revealed robust inflammatory cell infiltration, selective synthesis of IgG, in situ antigen driven B-cell clonal expansion, and deposition of immune complexes and complement proteins within CCM lesions. We aimed to evaluate the impact of suppressing the immune response on the formation and maturation of CCM lesions, as well as lesional iron deposition and ROCK activity. Two murine models of heterozygous Ccm3 (Pdcd10), which spontaneously develop CCM lesions with severe and milder phenotypes, were either untreated or received anti-mouse BR3 to deplete B cells. Brains from anti-mouse BR3-treated mice exhibited significantly fewer mature CCM lesions and smaller lesions compared to untreated mice. B cell depletion halted the progression of lesions into mature stage 2 lesions but did not prevent their genesis. Non-heme iron deposition and ROCK activity was decreased in lesions of B cell depleted mice. This represents the first report of the therapeutic benefit of B-cell depletion in the development and progression of CCMs, and provides a proof of principle that B cells play a critical role in CCM lesion genesis and maturation. These findings add biologics to the list of potential therapeutic agents for CCM disease. Future studies would characterize the putative antigenic trigger and further define the mechanism of immune response in the lesions.
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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.