ArticleThe Journal of clinical investigation2020
Myelin-specific CD8+ T cells exacerbate brain inflammation in CNS autoimmunity.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- Glatiramer Acetate Immunomodulation: Evidence of Neuroprotection and Cognitive Preservation.Cells · 2022Pooled it
- Review
- Neuroimmune interactions: from molecular mechanisms to therapeutic targets.Molecular biomedicine · 2026Review
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- RNA Helicase DDX21 Controls CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cross-presentation of citrullinated antigens drives cytotoxic CD8bioRxiv : the preprint server for biology · 2026Article
- CD11c+ CD8 T cells cause IFN-γ-dependent autoimmune neuroinflammation that is restrained by PD-1 signaling.JCI insight · 2026Article
- Microglial-Derived IGF-1 Serves as a Regulator for Neuroimmune Homeostasis During Viral-Induced Demyelination.Viruses · 2026Article
- Microglial HDAC3 inhibits the migration of CD8-positive T cell in the development of EAE by restraining the expression of CCL5.Cell & bioscience · 2026Article
- FKBP5 regulates interferon signaling leading to myeloid cell activation in multiple sclerosis.Journal of neuroinflammation · 2026Article
- Proteasome 20S beta 8 (PSMB8) as a metabolic switcher of neuronal ferroptosis in multiple sclerosis.Cell death and differentiation · 2026Article
- Redefining multiple sclerosis therapy through microbial immunomodulation and epigenetic control.Journal of translational autoimmunity · 2025Review
- White Blood Cells in Neurodegenerative Diseases in the Context of Neuroinflammation.Molecular neurobiology · 2025Review
- Acetyl 11-Keto Beta-Boswellic Acid Improves Neurological Functions in a Mouse Model of Multiple Sclerosis.Inflammation · 2025Article
- Pidotimod alleviated experimental autoimmune encephalomyelitis by regulating the balance of splenic lymphocytes.BMC immunology · 2025Article
- Enhancement of CD8Journal of translational autoimmunity · 2025Article
- Article
- Experimental autoimmune encephalomyelitis pathogenesis alters along animal age: impact of S100B expression.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Epstein-Barr virus infection promotes T cell dysregulation in a humanized mouse model of multiple sclerosis.Science advances · 2025Article
- Myelin-reactive CD8Journal of neuroinflammation · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the CNS. Although CD4+ T cells are implicated in MS pathogenesis and have been the main focus of MS research using the animal model experimental autoimmune encephalomyelitis (EAE), substantial evidence from patients with MS points to a role for CD8+ T cells in disease pathogenesis. We previously showed that an MHC class I-restricted epitope of myelin basic protein (MBP) is presented in the CNS during CD4+ T cell-initiated EAE. Here, we investigated whether naive MBP-specific CD8+ T cells recruited to the CNS during CD4+ T cell-initiated EAE engaged in determinant spreading and influenced disease. We found that the MBP-specific CD8+ T cells exacerbated brain but not spinal cord inflammation. We show that a higher frequency of monocytes and monocyte-derived cells presented the MHC class I-restricted MBP ligand in the brain compared with the spinal cord. Infiltration of MBP-specific CD8+ T cells enhanced ROS production in the brain only in these cell types and only when the MBP-specific CD8+ T cells expressed Fas ligand (FasL). These results suggest that myelin-specific CD8+ T cells may contribute to disease pathogenesis via a FasL-dependent mechanism that preferentially promotes lesion formation in the brain.
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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.