ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Immune deficiency in mouse models for inherited peripheral neuropathies leads to improved myelin maintenance.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. 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, 120 citations in OpenAlex.
- Article
- A Role of Inflammation in Charcot-Marie-Tooth Disorders-In a Perspective of Treatment?International journal of molecular sciences · 2024Review
- Demyelinating processes in aging and stroke in the central nervous system and the prospect of treatment strategy.CNS neuroscience & therapeutics · 2020Review
- Absence of Plekhg5 Results in Myelin Infoldings Corresponding to an Impaired Schwann Cell Autophagy, and a Reduced T-Cell Infiltration Into Peripheral Nerves.Frontiers in cellular neuroscience · 2020Article
- Review
- Endogenous antibodies contribute to macrophage-mediated demyelination in a mouse model for CMT1B.Journal of neuroinflammation · 2015Article
- Animal models of autoimmune neuropathy.ILAR journal · 2014Review
- Biochemical characterization of protein quality control mechanisms during disease progression in the C22 mouse model of CMT1A.ASN neuro · 2013Article
- Functional recovery of regenerating motor axons is delayed in mice heterozygously deficient for the myelin protein P(0) gene.Neurochemical research · 2013Article
- Peptide mimetic of the S100A4 protein modulates peripheral nerve regeneration and attenuates the progression of neuropathy in myelin protein P0 null mice.Molecular medicine (Cambridge, Mass.) · 2013Article
- Acute injury in the peripheral nervous system triggers an alternative macrophage response.Journal of neuroinflammation · 2012Article
- Inherited neuropathies.Current treatment options in neurology · 2011Article
- MCP-1/CCL2 modifies axon properties in a PMP22-overexpressing mouse model for Charcot-Marie-tooth 1A neuropathy.The American journal of pathology · 2010Article
- Genetically determined neuropathy (CMT 1A) accompanied by immune dysfunction: a case report.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009Article
- Article
- Experimental models of spontaneous autoimmune disease in the central nervous system.Journal of molecular medicine (Berlin, Germany) · 2007Review
- Immune cells contribute to myelin degeneration and axonopathic changes in mice overexpressing proteolipid protein in oligodendrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Role of immune cells in animal models for inherited peripheral neuropathies.Neuromolecular medicine · 2006Review
- Molecular genetics of autosomal-dominant demyelinating Charcot-Marie-Tooth disease.Neuromolecular medicine · 2006Review
- [The role of the immune system in hereditary demyelinating neuropathies].Der Nervenarzt · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adhesive cell surface molecule P(0) is the most abundant glycoprotein in peripheral nerve myelin and fulfills pivotal functions during myelin formation and maintenance. Mutations in the corresponding gene cause hereditary demyelinating neuropathies. In mice heterozygously deficient in P(0) (P(0)(+/-) mice), an established animal model for a subtype of hereditary neuropathies, T-lymphocytes are present in the demyelinating nerves. To monitor the possible involvement of the immune system in myelin pathology, we cross-bred P(0)(+/-) mice with null mutants for the recombination activating gene 1 (RAG-1) or with mice deficient in the T-cell receptor alpha-subunit. We found that in P(0)(+/-) mice myelin degeneration and impairment of nerve conduction properties is less severe when the immune system is deficient. Moreover, isolated T-lymphocytes from P(0)(+/-) mice show enhanced reactivity to myelin components of the peripheral nerve, such as P(0), P(2), and myelin basic protein. We hypothesize that autoreactive immune cells can significantly foster the demyelinating phenotype of mice with a primarily genetically based peripheral neuropathy.
Indexed as
Identifiers
10632602PMC6772400W1609207043What OpenQuestion holds
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.