ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Interleukin-6 protects anterior horn neurons from lethal virus-induced injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Interleukin-6 Expression by Hypothalamic Microglia in Multiple Inflammatory Contexts: A Systematic Review.BioMed research international · 2019Pooled it
- The Role of IL-6 in Neurodegenerative Disorders.Neurochemical research · 2024Review
- Article
- A Major Downregulation of Circulating microRNAs in Zika Acutely Infected Patients: Potential Implications in Innate and Adaptive Immune Response Signaling Pathways.Frontiers in genetics · 2022Article
- Genetic and immunological contributors to virus-induced paralysis.Brain, behavior, & immunity - health · 2021Article
- Suppression of interleukin-6 increases enterovirus A71 lethality in mice.Journal of biomedical science · 2017Article
- Molecular mechanisms of neuroinflammation and injury during acute viral encephalitis.Journal of neuroimmunology · 2017Review
- Decreased Motor Neuron Support by SMA Astrocytes due to Diminished MCP1 Secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Human class I major histocompatibility complex alleles determine central nervous system injury versus repair.Journal of neuroinflammation · 2016Article
- Antibody-Mediated Oligodendrocyte Remyelination Promotes Axon Health in Progressive Demyelinating Disease.Molecular neurobiology · 2016Review
- Beyond muscles: The untapped potential of creatine.International immunopharmacology · 2016Review
- 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
- The role of the JAK-STAT pathway in neural stem cells, neural progenitor cells and reactive astrocytes after spinal cord injury.Biomedical reports · 2015Article
- Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.Journal of neurology & translational neuroscience · 2014Article
- An elite controller of picornavirus infection targets an epitope that is resistant to immune escape.PloS one · 2014Article
- The epitope integration site for vaccine antigens determines virus control while maintaining efficacy in an engineered cancer vaccine.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Control of early Theiler's murine encephalomyelitis virus replication in macrophages by interleukin-6 occurs in conjunction with STAT1 activation and nitric oxide production.Journal of virology · 2012Article
- Deletion of beta-2-microglobulin ameliorates spinal cord lesion load and promotes recovery of brainstem NAA levels in a murine model of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2012Article
- Prevention of methamphetamine-induced microglial cell death by TNF-α and IL-6 through activation of the JAK-STAT pathway.Journal of neuroinflammation · 2012Article
- Two discreet subsets of CD8 T cells modulate PLP(91-110) induced experimental autoimmune encephalomyelitis in HLA-DR3 transgenic mice.Journal of autoimmunity · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We evaluated the role of interleukin-6 (IL-6) in neuronal injury after CNS infection. IL-6-/- and IL-6+/+ mice of resistant major histocompatibility complex (MHC) H-2b haplotype intracerebrally infected with Theiler's virus cleared the infection normally without development of viral persistence, lethal neuronal infection, or late phase demyelination. In contrast, infection of IL-6-/- mice on a susceptible H-2q haplotype resulted in frequent deaths and severe neurologic deficits within 2 weeks of infection as compared with infected IL-6+/+ H-2q littermate controls. Morphologic analysis demonstrated dramatic injury to anterior horn neurons of IL-6-/- H-2q mice at 12 d after infection. Infectious viral titers in the CNS (brain and spinal cord combined) were equivalent between IL-6-/- H-2q and IL-6+/+ H-2q mice. In contrast, more viral RNA was detected in the spinal cord of IL-6-/- mice compared with IL-6+/+ H-2q mice. Virus antigen was localized predominantly to anterior horn cells in infected IL-6-/- H-2q mice. IL-6 deletion did not affect the humoral response directed against virus, nor did it affect the expression of CD4, CD8, MHC class I, or MHC class II in the CNS. Importantly, IL-6 was expressed by astrocytes of infected IL-6+/+ mice but not in astrocytes of IL-6-/- mice or uninfected IL-6+/+ mice. Furthermore, expression of various chemokines was robust at 12 d after infection in both H-2b and H-2q IL-6-/- mice, indicating that intrinsic CNS inflammatory responses did not depend on the presence of IL-6. Finally, in vitro analysis of virus-induced death in neuroblastoma-spinal cord-34 motor neurons and primary anterior horn cell neurons showed that IL-6 exerted a neuroprotective effect. These data support the hypothesis that IL-6 plays a critical role in protecting specific populations of neurons from irreversible injury.
Indexed as
Identifiers
12533608PMC6741877W1822012598What 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.