ArticleJournal of neurology2009
Development of ALS-like disease in SOD-1 mice deficient of B lymphocytes.
Article in Journal of neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 43 citations in OpenAlex.
- White Blood Cells in Neurodegenerative Diseases in the Context of Neuroinflammation.Molecular neurobiology · 2025Review
- Engineering neuroimmune regulation: biomaterial and nanotechnology platforms for neuropathology diagnosis and targeted immunomodulation.Frontiers in immunology · 2025Review
- The contribution of the peripheral immune system to neurodegeneration.Nature neuroscience · 2023Review
- Senescent-like Blood Lymphocytes and Disease Progression in Amyotrophic Lateral Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- CSF oligoclonal IgG bands are not associated with ALS progression and prognosis.Frontiers in neurology · 2023Article
- T cell responses at diagnosis of amyotrophic lateral sclerosis predict disease progression.Nature communications · 2022Article
- Advances on Cellular Clonotypic Immunity in Amyotrophic Lateral Sclerosis.Brain sciences · 2022Review
- Sublethal enteroviral infection exacerbates disease progression in an ALS mouse model.Journal of neuroinflammation · 2022Article
- Neuroimmune Crosstalk Between the Peripheral and the Central Immune System in Amyotrophic Lateral Sclerosis.Frontiers in aging neuroscience · 2022Review
- Interplay between immunity and amyotrophic lateral sclerosis: Clinical impact.Neuroscience and biobehavioral reviews · 2021Review
- Review
- Neuroinflammation in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia and the Interest of Induced Pluripotent Stem Cells to Study Immune Cells Interactions With Neurons.Frontiers in molecular neuroscience · 2021Review
- CXCL13/CXCR5 signalling is pivotal to preserve motor neurons in amyotrophic lateral sclerosis.EBioMedicine · 2020Article
- Modifying macrophages at the periphery has the capacity to change microglial reactivity and to extend ALS survival.Nature neuroscience · 2020Article
- SOD1 suppresses pro-inflammatory immune responses by protecting against oxidative stress in colitis.Redox biology · 2020Article
- Aging and Neurodegenerative Disease: Is the Adaptive Immune System a Friend or Foe?Frontiers in aging neuroscience · 2020Review
- Immunity in amyotrophic lateral sclerosis: blurred lines between excessive inflammation and inefficient immune responses.Brain communications · 2020Review
- Plasma Inflammatory Cytokines Are Elevated in ALS.Frontiers in neurology · 2020Article
- New insights into SMA pathogenesis: immune dysfunction and neuroinflammation.Annals of clinical and translational neurology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several recent studies proposed a role for innate immunity and inflammation in the pathogenesis of amyotrophic lateral sclerosis (ALS). However, possible links, if any, between disease and adaptive immunity are poorly understood. The present study probed for the role of B cells in ALS disease using the G93A-SOD-1 transgenic mouse model. In agreement with other studies, we show here that autoantibodies are detectable in SOD-1 mice. However, SOD-1 B cells did not express any altered phenotype and exhibited indistinguishable responsiveness to immunogenic stimuli relative to wild-type B cells. This was obtained for B cells isolated before, during and after the onset of ALS-like disease. Finally, to obtain an in vivo conclusion, we generated SOD-1 mice that are deficient of B cells, by crossing SOD-1 mice with Igmu-deficient mice (muMT), where B cell development is blocked at the proB stage. The meteoric assays performed on a rota-rod clearly showed the development of ALS-like disease in SOD-1 mice that are deficient of B cells not differently than in control SOD-1 mice. Our results propose that B lymphocytes do not have a major role in the pathogenesis of ALS-like disease in SOD-1 mice.
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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.