ArticleJournal of immunology (Baltimore, Md. : 1950)2015
B cell antigen presentation is sufficient to drive neuroinflammation in an animal model of multiple sclerosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
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Who cites it
59 citing papers in PubMed, 98 citations in OpenAlex.
- Dynamics of Spinal Fluid Immune Cell Alterations Following Cladribine Tablet Treatment in Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2026Trial
- Modeling pathogenic B cell function in experimental autoimmune encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Turncoat antibodies unmasked in a model of autoimmune demyelination: From biology to therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Potential mechanisms linking bacterial factors to the development and progression of multiple sclerosis.Infectious medicine · 2025Review
- B cell-mediated antigen presentation promotes adverse cardiac remodeling in chronic heart failure.Research square · 2024Article
- A B cell-driven EAE mouse model reveals the impact of B cell-derived cytokines on CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Pathogenic Role of Fibrinogen in the Neuropathology of Multiple Sclerosis: A Tale of Sorrows and Fears.Neurochemical research · 2023Review
- Proteolipid Protein-Induced Mouse Model of Multiple Sclerosis Requires B Cell-Mediated Antigen Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Recent Progress in Multiple Sclerosis Treatment Using Immune Cells as Targets.Pharmaceutics · 2023Review
- Dual Role of B Cells in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- A quinazoline derivative suppresses B cell hyper-activation and ameliorates the severity of systemic lupus erythematosus in mice.Frontiers in pharmacology · 2023Article
- SLAMF7 modulates B cells and adaptive immunity to regulate susceptibility to CNS autoimmunity.Journal of neuroinflammation · 2022Article
- CD11bJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Preclinical Analysis of Candidate Anti-Human CD79 Therapeutic Antibodies Using a Humanized CD79 Mouse Model.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Targeting IFN-λ Signaling Promotes Recovery from Central Nervous System Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Neuroinflammation and Proinflammatory Cytokines in Epileptogenesis.Molecular neurobiology · 2022Review
- The Ins and Outs of Antigen Uptake in B cells.Frontiers in immunology · 2022Review
- Dopaminergic stimulation leads B-cell infiltration into the central nervous system upon autoimmunity.Journal of neuroinflammation · 2021Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
B cells are increasingly regarded as integral to the pathogenesis of multiple sclerosis, in part as a result of the success of B cell-depletion therapy. Multiple B cell-dependent mechanisms contributing to inflammatory demyelination of the CNS have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T cell-dependent animal model for multiple sclerosis. Although B cell Ag presentation was suggested to regulate CNS inflammation during EAE, direct evidence that B cells can independently support Ag-specific autoimmune responses by CD4 T cells in EAE is lacking. Using a newly developed murine model of in vivo conditional expression of MHC class II, we reported previously that encephalitogenic CD4 T cells are incapable of inducing EAE when B cells are the sole APC. In this study, we find that B cells cooperate with dendritic cells to enhance EAE severity resulting from myelin oligodendrocyte glycoprotein (MOG) immunization. Further, increasing the precursor frequency of MOG-specific B cells, but not the addition of soluble MOG-specific Ab, is sufficient to drive EAE in mice expressing MHCII by B cells alone. These data support a model in which expansion of Ag-specific B cells during CNS autoimmunity amplifies cognate interactions between B and CD4 T cells and have the capacity to independently drive neuroinflammation at later stages of disease.
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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.