ArticleAnnals of neurology2015
B-cell very late antigen-4 deficiency reduces leukocyte recruitment and susceptibility to central nervous system autoimmunity.
Article in Annals of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed.
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.Frontiers in cellular neuroscience · 2026Review
- Immune conversations at the border: meningeal immunity in health and disease.Frontiers in immunology · 2025Review
- CAR-T Cell-Mediated B-Cell Depletion in Central Nervous System Autoimmunity.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Microglia and meningeal macrophages depletion delays the onset of experimental autoimmune encephalomyelitis.Cell death & disease · 2023Article
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- B cells in central nervous system disease: diversity, locations and pathophysiology.Nature reviews. Immunology · 2022Review
- Breaching Brain Barriers: B Cell Migration in Multiple Sclerosis.Biomolecules · 2022Review
- Dopaminergic stimulation leads B-cell infiltration into the central nervous system upon autoimmunity.Journal of neuroinflammation · 2021Article
- Skin-Homing Regulatory B Cells Required for Suppression of Cutaneous Inflammation.The Journal of investigative dermatology · 2021Article
- Effects of Natalizumab Therapy on Intrathecal Immunoglobulin G Production Indicate Targeting of Plasmablasts.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- The role of B cells in the immunopathogenesis of multiple sclerosis.Immunology · 2020Review
- VLA-4 Expression and Activation in B Cell Malignancies: Functional and Clinical Aspects.International journal of molecular sciences · 2020Review
- Article
- B and T Cells Driving Multiple Sclerosis: Identity, Mechanisms and Potential Triggers.Frontiers in immunology · 2020Review
- The Choroid Plexus Is Permissive for a Preactivated Antigen-Experienced Memory B-Cell Subset in Multiple Sclerosis.Frontiers in immunology · 2020Article
- Neutrophils promote VLA-4-dependent B cell antigen presentation and accumulation within the meninges during neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Effects of natalizumab therapy on intrathecal antiviral antibody responses in MS.Neurology(R) neuroimmunology & neuroinflammation · 2019Observational
- The Multiple Roles of B Cells in Multiple Sclerosis and Their Implications in Multiple Sclerosis Therapies.Cold Spring Harbor perspectives in medicine · 2019Review
- B-Cell Therapies in Multiple Sclerosis.Cold Spring Harbor perspectives in medicine · 2019Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Natalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for multiple sclerosis (MS). Studies have focused primarily upon its capacity to interfere with T-cell migration into the central nervous system (CNS). B cells are important in MS pathogenesis and express high levels of VLA-4. Here, we report that the selective inhibition of VLA-4 expression on B cells impedes CNS accumulation of B cells, and recruitment of Th17 cells and macrophages, and reduces susceptibility to experimental autoimmune encephalomyelitis. These results underscore the importance of B-cell VLA-4 expression in the pathogenesis of CNS autoimmunity and provide insight regarding mechanisms that may contribute to the benefit of natalizumab in MS, as well as candidate therapeutics that selectively target B cells.
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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.