ArticleExperimental neurology2016
Peripheral and central neuronal ATF3 precedes CD4+ T-cell infiltration in EAE.
Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- EAE models of neuropathic pain in multiple sclerosis do not require pertussis toxin.Brain research · 2026Article
- Siponimod treatment response shows partial BDNF dependency in multiple sclerosis models.Scientific reports · 2024Article
- Discovery of a CCR2-targeting pepducin therapy for chronic pain.Pharmacological research · 2024Article
- Shared Molecular Signatures Across Zika Virus Infection and Multiple Sclerosis Highlight AP-1 Transcription Factor as a Potential Player in Post-ZIKV MS-Like Phenotypes.Molecular neurobiology · 2023Article
- Effects of perinatal exposure to bisphenol A or S in EAE model of multiple sclerosis.Cell and tissue research · 2023Article
- Strain and sex differences in somatosensation and sociability during experimental autoimmune encephalomyelitis.Brain, behavior, & immunity - health · 2021Article
- N-Acylethanolamine-Hydrolyzing Acid Amidase Inhibition, but Not Fatty Acid Amide Hydrolase Inhibition, Prevents the Development of Experimental Autoimmune Encephalomyelitis in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis.Journal of neuroinflammation · 2020Article
- Article
- A TLR-CXCL1 pathway in DRG neurons induces neutrophil accumulation in the DRG and mechanical allodynia in EAE mice.Scientific reports · 2019Article
- Regulatory T Cells and Their Derived Cytokine, Interleukin-35, Reduce Pain in Experimental Autoimmune Encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Review
- IGF-1 Via PI3K/Akt/S6K Signaling Pathway Protects DRG Neurons with High Glucose-induced Toxicity.Open life sciences · 2019Article
- Cyclic AMP Pathway Suppress Autoimmune Neuroinflammation by Inhibiting Functions of Encephalitogenic CD4 T Cells and Enhancing M2 Macrophage Polarization at the Site of Inflammation.Frontiers in immunology · 2018Article
- Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease.Journal of neuroinflammation · 2017Article
- Peripheral sensory neuron injury contributes to neuropathic pain in experimental autoimmune encephalomyelitis.Scientific reports · 2017Article
- Cutaneous tissue damage induces long-lasting nociceptive sensitization and regulation of cellular stress- and nerve injury-associated genes in sensory neurons.Experimental neurology · 2016Article
- Peripheral and Central Neuroinflammatory Changes and Pain Behaviors in an Animal Model of Multiple Sclerosis.Frontiers in immunology · 2016Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis produced by immunization with myelin oligodendrocyte glycoprotein (MOG) and adjuvants, results from profound T-cell mediated CNS demyelination. EAE is characterized by progressive, ascending motor dysfunction and symptoms of ongoing pain and hypersensitivity, in some cases preceding or concomitant with the motor deficits. In this regard, the EAE model mimics major features of multiple sclerosis, where a central neuropathic pain state is common. Although the latter condition is presumed to arise from a CNS loss of inhibitory controls secondary to the demyelination, dysfunction of sensory neurons may also contribute. Based on our previous studies that demonstrated the utility of monitoring expression of activating transcription factor 3 (ATF3), a sensitive marker of injured sensory neurons, here we followed both ATF3 and CD4+ T cells invasion of sensory ganglia (as well as the CNS) at different stages of the EAE model. We found that ATF3 is induced in peripheral sensory ganglia and brainstem well before the appearance of motor deficits. Unexpectedly, the ATF3 induction always preceded T cell infiltration, typically in adjacent, but non-overlapping regions. Surprisingly, control administration of the pertussis toxin and/or Complete Freund's adjuvants, without MOG, induced ATF3 in sensory neurons. In contrast, T cell infiltration only occurred with MOG. Taken together, our results suggest that the clinical manifestations in the EAE result not only from central demyelination but also from neuronal stress and subsequent pathophysiology of sensory neurons.
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