ArticleiScience2022
Immune-mediated neurodegenerative trait provoked by multimodal derepression of long-interspersed nuclear element-1.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Coincidence of L1 retrotransposition and DNA repair deficiency elicits synthetic lethality in S-phase mature neurons.iScience · 2026Article
- Article
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Article
- Exploring the Relationship of Transposable Elements and Ageing: Causes and Consequences.Genome biology and evolution · 2025Review
- Transposon activity and nucleotide triplet instability: new perspectives on their potential interplay in brain disorders.Frontiers in neuroscience · 2025Article
- Dynamic dysregulation of retrotransposons in neurodegenerative diseases at the single-cell level.Genome research · 2024Article
- iPS cell generation-associated point mutations include many C > T substitutions via different cytosine modification mechanisms.Nature communications · 2024Article
- Eomesodermin expression in CD4CNS neuroscience & therapeutics · 2024Article
- Terminally differentiated cytotoxic CD4CNS neuroscience & therapeutics · 2024Article
- Pathogenic Microglia Orchestrate Neurotoxic Properties of Eomes-Expressing Helper T Cells.Cells · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegeneration is a process involving both cell autonomous and non-cell autonomous neuron loss, followed by a collapse of neural networks, but its pathogenesis is poorly understood. We have previously demonstrated that Eomes-positive helper T (Eomes + Th) cells recognizing LINE-1(L1)-derived prototypic antigen ORF1 mediate neurotoxicity associated with the neurodegenerative pathology of experimental autoimmune encephalomyelitis (EAE). Here, we show that Eomes + Th cells accumulate in the CNS of mouse models of authentic neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD), and secrete the neurotoxic granzyme B after encounter with ORF1 antigen. Multimodal derepression of neuronal L1 transcription is observed in EAE and ALS/AD models during neurodegeneration in active and cell cycle-mediated manner, respectively. These data suggest that the adventitious concurrence of immune-mediated neurodegenerative traits by Eomes + Th cells and ectopic expression of L1-derived antigen(s) in the inflamed CNS may materialize a communal and previously unappreciated pathogenesis of neurodegeneration.
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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.