ArticleFrontiers in immunology2015
Meningeal Infiltration of the Spinal Cord by Non-Classically Activated B Cells is Associated with Chronic Disease Course in a Spontaneous B Cell-Dependent Model of CNS Autoimmune Disease.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
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- Anti-MOG IgG in EAE models clinical aspects of pediatric MOGAD.Frontiers in immunology · 2026Article
- 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
- Follicle on the Roof: Tertiary Lymphoid Structures in Central Nervous System Autoimmunity.Immunological reviews · 2025Review
- Tertiary Lymphoid Structures in Central Nervous System Disorders.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Persistent virus-specific and clonally expanded antibody-secreting cells respond to induced self-antigen in the CNS.Acta neuropathologica · 2023Article
- Lymphotoxin-alpha expression in the meninges causes lymphoid tissue formation and neurodegeneration.Brain : a journal of neurology · 2022Article
- B cells in central nervous system disease: diversity, locations and pathophysiology.Nature reviews. Immunology · 2022Review
- Novel contributors to B cell activation during inflammatory CNS demyelination; An oNGOing process.International journal of medical sciences · 2022Review
- Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Anti-CD20 Depletes Meningeal B Cells but Does Not Halt the Formation of Meningeal Ectopic Lymphoid Tissue.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Meningeal B Cell Clusters Correlate with Submeningeal Pathology in a Natural Model of Multiple Sclerosis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Tertiary Lymphoid Structures in the Central Nervous System: Implications for Glioblastoma.Frontiers in immunology · 2021Review
- 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
- The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain.Immunotherapy · 2019Review
- Central Nervous System Inflammatory Aggregates in the Theiler's Virus Model of Progressive Multiple Sclerosis.Frontiers in immunology · 2019Article
- FUS(1-359) transgenic mice as a model of ALS: pathophysiological and molecular aspects of the proteinopathy.Neurogenetics · 2018Article
- Demyelination in Multiple Sclerosis: Reprogramming Energy Metabolism and Potential PPARγ Agonist Treatment Approaches.International journal of molecular sciences · 2018Review
- Tertiary Lymphoid Structures: Autoimmunity Goes Local.Frontiers in immunology · 2018Review
- An optimized method for enumerating CNS derived memory B cells during viral-induced inflammation.Journal of neuroscience methods · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We characterized B cell infiltration of the spinal cord in a B cell-dependent spontaneous model of central nervous system (CNS) autoimmunity that develops in a proportion of mice with mutant T and B cell receptors specific for myelin oligodendrocyte glycoprotein. We found that, while males are more likely to develop disease, females are more likely to have a chronic rather than monophasic disease course. B cell infiltration of the spinal cord was investigated by histology and FACs. CD4(+) T cell infiltration was pervasive throughout the white and in some cases gray matter. B cells were almost exclusively restricted to the meninges, often in clusters reminiscent of those described in human multiple sclerosis. These clusters were typically found adjacent to white matter lesions and their presence was associated with a chronic disease course. Extensive investigation of these clusters by histology did not identify features of lymphoid follicles, including organization of T and B cells into separate zones, CD35(+) follicular dendritic cells, or germinal centers. The majority of cluster B cells were IgD(+) with little evidence of class switch. Consistent with this, B cells isolated from the spinal cord were of the naïve/memory CD38(hi) CD95(lo) phenotype. Nevertheless, they were CD62L(lo) and CD80(hi) compared to lymph node B cells suggesting that they were at least partly activated and primed to present antigen. Therefore, if meningeal B cells contribute to CNS pathology in autoimmunity, follicular differentiation is not necessary for the pathogenic mechanism.
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