ArticleNeurobiology of disease2013
Axons are injured by antigen-specific CD8(+) T cells through a MHC class I- and granzyme B-dependent mechanism.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Pentose phosphate pathway inhibition metabolically reprograms CD8+ T cells and disrupts CNS autoimmunity.JCI insight · 2025Article
- T Cells Trafficking into the Brain in Aging and Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Cerebral clues: serum neurofilament light chain (sNfL) as a novel biomarker for immune check point inhibitor (ICI) mediated seronegative encephalitis.Oxford medical case reports · 2024Article
- CD8+ T cells recognizing a neuron-restricted antigen injure axons in a model of multiple sclerosis.The Journal of clinical investigation · 2023Article
- Mechanisms underlying the beneficial effects of physical exercise on multiple sclerosis: focus on immune cells.Frontiers in immunology · 2023Review
- Brain Atrophy as an Outcome of Disease-Modifying Therapy for Remitting-Relapsing Multiple Sclerosis.Multiple sclerosis international · 2023Review
- ISGylation is induced in neurons by demyelination driving ISG15-dependent microglial activation.Journal of neuroinflammation · 2022Article
- Thinking outside the box: non-canonical targets in multiple sclerosis.Nature reviews. Drug discovery · 2022Review
- Cytotoxic B Cells in Relapsing-Remitting Multiple Sclerosis Patients.Frontiers in immunology · 2022Article
- T cell transgressions: Tales of T cell form and function in diverse disease states.International reviews of immunology · 2022Review
- Differential Cytokine-Induced Responses of Polarized Microglia.Brain sciences · 2021Article
- Double-edged effects of tamoxifen-in-oil-gavage on an infectious murine model for multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2021Article
- The CD8 T Cell-Epstein-Barr Virus-B Cell Trialogue: A Central Issue in Multiple Sclerosis Pathogenesis.Frontiers in immunology · 2021Review
- Remyelination-Promoting DNA Aptamer Conjugate Myaptavin-3064 Binds to Adult Oligodendrocytes In Vitro.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Cytotoxic Immunity in Peripheral Nerve Injury and Pain.Frontiers in neuroscience · 2020Review
- Robust Control of a Brain-Persisting Parasite through MHC I Presentation by Infected Neurons.Cell reports · 2019Article
- A Pilot Study Identifying Brain-Targeting Adaptive Immunity in Pediatric Extracorporeal Membrane Oxygenation Patients With Acquired Brain Injury.Critical care medicine · 2019Observational
- Microfluidic platforms for the study of neuronal injury in vitro.Biotechnology and bioengineering · 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
- A Novel Association of Polymorphism in theMediators of inflammation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Axon injury is a central determinant of irreversible neurological deficit and disease progression in patients with multiple sclerosis (MS). CD8(+) lymphocytes (CTLs) within inflammatory demyelinated MS lesions correlate with acute axon injury and neurological deficits. The mechanisms of these correlations are unknown. We interrogated CTL-mediated axon injury using the transgenic OT-I antigen-specific CTL model system in conjunction with a chambered cortical neuron culture platform that permitted the isolated manipulation of axons independent of neuron cell bodies and glia. Interferon gamma upregulated, through a dose dependent mechanism, the axonal expression of functional major histocompatibility complex class I (MHC I) molecules competent to present immunologically-relevant antigens derived from endogenously expressed proteins. Antigen-specific CTLs formed cytotoxic immune synapses with and directly injured axons expressing antigen-loaded MHC I molecules. CTL-mediated axon injury was mechanistically dependent upon axonal MHC I antigen presentation, T cell receptor specificity and axoplasmic granzyme B activity. Despite extensive distal CTL-mediated axon injury, acute neuron cell body apoptosis was not observed. These findings present a novel model of immune-mediated axon injury and offer anti-axonal CTLs and granzyme B as targets for the therapeutic protection of axons and prevention of neurological deficits in MS patients.
Indexed as
Identifiers
What 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.