ArticlePloS one2018
B cells are capable of independently eliciting rapid reactivation of encephalitogenic CD4 T cells in a murine model of multiple sclerosis.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 22 citations in OpenAlex.
- From Demyelination to Intervention: Natural Compounds as Emerging Therapeutic Targets in Multiple Sclerosis Neuroinflammation.Journal of immunology research · 2026Review
- The Plasticity of Immune Cell Response Complicates Dissecting the Underlying Pathology of Multiple Sclerosis.Journal of immunology research · 2024Review
- The role of fibronectin in multiple sclerosis and the effect of drug delivery across the blood-brain barrier.Neural regeneration research · 2023Review
- Proteolipid Protein-Induced Mouse Model of Multiple Sclerosis Requires B Cell-Mediated Antigen Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- B cells in central nervous system disease: diversity, locations and pathophysiology.Nature reviews. Immunology · 2022Review
- Effects of a Fully Humanized Type II Anti-CD20 Monoclonal Antibody on Peripheral and CNS B Cells in a Transgenic Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2022Article
- Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target.Frontiers in immunology · 2022Review
- Correlation between the Neutrophil-to-Lymphocyte Ratio and Multiple Sclerosis: Recent Understanding and Potential Application Perspectives.Neurology research international · 2022Review
- Dopaminergic stimulation leads B-cell infiltration into the central nervous system upon autoimmunity.Journal of neuroinflammation · 2021Article
- Novel B cell-dependent multiple sclerosis model using extracellular domains of myelin proteolipid protein.Scientific reports · 2020Article
- B Cells in Multiple Sclerosis and Virus-Induced Neuroinflammation.Frontiers in neurology · 2020Review
- B cells in autoimmune and neurodegenerative central nervous system diseases.Nature reviews. Neuroscience · 2019Review
- 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
- Non-Antibody-Secreting Functions of B Cells and Their Contribution to Autoimmune Disease.Annual review of cell and developmental biology · 2019Review
- The Diversity of Encephalitogenic CD4+ T Cells in Multiple Sclerosis and Its Animal Models.Journal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recent success with B cell depletion therapies has revitalized efforts to understand the pathogenic role of B cells in Multiple Sclerosis (MS). Using the adoptive transfer system of experimental autoimmune encephalomyelitis (EAE), a murine model of MS, we have previously shown that mice in which B cells are the only MHCII-expressing antigen presenting cell (APC) are susceptible to EAE. However, a reproducible delay in the day of onset of disease driven by exclusive B cell antigen presentation suggests that B cells require optimal conditions to function as APCs in EAE. In this study, we utilize an in vivo genetic system to conditionally and temporally regulate expression of MHCII to test the hypothesis that B cell APCs mediate attenuated and delayed neuroinflammatory T cell responses during EAE. Remarkably, induction of MHCII on B cells following the transfer of encephalitogenic CD4 T cells induced a rapid and robust form of EAE, while no change in the time to disease onset occurred for recipient mice in which MHCII is induced on a normal complement of APC subsets. Changes in CD4 T cell activation over time did not account for more rapid onset of EAE symptoms in this new B cell-mediated EAE model. Our system represents a novel model to study how the timing of pathogenic cognate interactions between lymphocytes facilitates the development of autoimmune attacks within the CNS.
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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.