ArticleNeurobiology of disease2007
Absence of perforin expression confers axonal protection despite demyelination.
Article in Neurobiology of disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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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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
40 citing papers in PubMed, 61 citations in OpenAlex.
- Pentose phosphate pathway inhibition metabolically reprograms CD8+ T cells and disrupts CNS autoimmunity.JCI insight · 2025Article
- Identification of crucial inflammaging related risk factors in multiple sclerosis.Frontiers in molecular neuroscience · 2024Article
- CD8+ T cells recognizing a neuron-restricted antigen injure axons in a model of multiple sclerosis.The Journal of clinical investigation · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Multiple Sclerosis: Mechanisms of Disease and Strategies for Myelin and Axonal Repair.Neurologic clinics · 2018Review
- Retrograde interferon-gamma signaling induces major histocompatibility class I expression in human-induced pluripotent stem cell-derived neurons.Annals of clinical and translational neurology · 2018Article
- Multiple sclerosis: experimental models and reality.Acta neuropathologica · 2017Review
- A monoclonal natural human IgM protects axons in the absence of remyelination.Journal of neuroinflammation · 2016Article
- A single dose of a neuron-binding human monoclonal antibody improves brainstem NAA concentrations, a biomarker for density of spinal cord axons, in a model of progressive multiple sclerosis.Journal of neuroinflammation · 2015Article
- Organ-specific protective role of NKT cells in virus-induced inflammatory demyelination and myocarditis depends on mouse strain.Journal of neuroimmunology · 2015Article
- Article
- Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.Journal of neurology & translational neuroscience · 2014Article
- Axons are injured by antigen-specific CD8(+) T cells through a MHC class I- and granzyme B-dependent mechanism.Neurobiology of disease · 2013Article
- Promoting return of function in multiple sclerosis: An integrated approach.Multiple sclerosis and related disorders · 2013Article
- CD8(+) T cells in multiple sclerosis.Expert opinion on therapeutic targets · 2013Review
- Profile of Circulatory Metabolites in a Relapsing-remitting Animal Model of Multiple Sclerosis using Global Metabolomics.Journal of clinical & cellular immunology · 2013Article
- Pathoetiology of multiple sclerosis: are we barking up the wrong tree?F1000prime reports · 2013Article
- Immunity and inflammation in neurodegenerative diseases.American journal of neurodegenerative disease · 2013Article
- Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis.Journal of neuroinflammation · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Current evidence suggests that demyelination may be a necessary but not a sufficient condition for neurologic deficits associated with multiple sclerosis. Axon injury that occurs within the permissive environment of the demyelinated lesion is better correlated with functional deficits, but the mechanisms and cellular effectors of this injury are largely unknown. In an effort to identify potential axon injury mediators, we examined demyelination, motor function, and the number of spinal axons in perforin-deficient mice. Perforin is a critical molecular mediator of cytotoxic immunological injury and we hypothesized that genetic deletion of perforin expression would protect demyelinated axons. Indeed, we found that while perforin-deficient mice had considerable spinal cord demyelination 180 days after infection with Theiler's murine encephalomyelitis virus, such mice exhibited functional and axonal preservation comparable to non-demyelinated perforin-competent controls. We conclude that perforin-dependent effector cells such as cytotoxic T cells, gammadelta T cells, and natural killer cells may play a role in axon damage that is dependent upon but separable from demyelination.
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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.