ArticleMediators of inflammation2013
Persistent inflammation in the CNS during chronic EAE despite local absence of IL-17 production.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Changes in structural plasticity of hippocampal neurons in an animal model of multiple sclerosis.Zoological research · 2024Article
- Methyl-CpG-Binding Protein 2 Emerges as a Central Player in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders.Cellular and molecular neurobiology · 2023Review
- Astrocyte interferon-gamma signaling dampens inflammation during chronic central nervous system autoimmunity via PD-L1.Journal of neuroinflammation · 2023Article
- The antimicrobial peptide cathelicidin drives development of experimental autoimmune encephalomyelitis in mice by affecting Th17 differentiation.PLoS biology · 2022Article
- CEST MRI and MALDI imaging reveal metabolic alterations in the cervical lymph nodes of EAE mice.Journal of neuroinflammation · 2022Article
- TRPV2: A Key Player in Myelination Disorders of the Central Nervous System.International journal of molecular sciences · 2022Article
- Dopaminergic Receptors as Neuroimmune Mediators in Experimental Autoimmune Encephalomyelitis.Molecular neurobiology · 2021Article
- MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge.Scientific reports · 2021Article
- Pathological pain processing in mouse models of multiple sclerosis and spinal cord injury: contribution of plasma membrane calcium ATPase 2 (PMCA2).Journal of neuroinflammation · 2019Article
- Analogues of ERβ ligand chloroindazole exert immunomodulatory and remyelinating effects in a mouse model of multiple sclerosis.Scientific reports · 2019Article
- Pramipexole, a Dopamine D2/D3 Receptor-Preferring Agonist, Prevents Experimental Autoimmune Encephalomyelitis Development in Mice.Molecular neurobiology · 2017Article
- pVAXhsp65 Vaccination Primes for High IL-10 Production and Decreases Experimental Encephalomyelitis Severity.Journal of immunology research · 2017Article
- Intracranial delivery of interleukin-17A via adeno-associated virus fails to induce physical and learning disabilities and neuroinflammation in mice but improves glucose metabolism through AKT signaling pathway.Brain, behavior, and immunity · 2016Article
- Sustained TNF production by central nervous system infiltrating macrophages promotes progressive autoimmune encephalomyelitis.Journal of neuroinflammation · 2016Article
- Moringin activates Wnt canonical pathway by inhibiting GSK3β in a mouse model of experimental autoimmune encephalomyelitis.Drug design, development and therapy · 2016Article
- A new formulation of cannabidiol in cream shows therapeutic effects in a mouse model of experimental autoimmune encephalomyelitis.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2015Article
- Article
- Experimental autoimmune encephalomyelitis development is aggravated by Candida albicans infection.Journal of immunology research · 2015Article
- Treatment with Vitamin D/MOG Association Suppresses Experimental Autoimmune Encephalomyelitis.PloS one · 2015Article
- Copaiba oil suppresses inflammatory cytokines in splenocytes of C57Bl/6 mice induced with experimental autoimmune encephalomyelitis (EAE).Molecules (Basel, Switzerland) · 2014Article
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8 authors.
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Abstract
Experimental autoimmune encephalomyelitis (EAE) is an artificially induced demyelination of the central nervous system (CNS) that resembles multiple sclerosis in its clinical, histopathological, and immunological features. Activated Th1 and Th17 cells are thought to be the main immunological players during EAE development. This study was designed to evaluate peripheral and local contribution of IL-17 to acute and chronic EAE stages. C57BL/6 mice were immunized with MOG plus complete Freund's adjuvant followed by pertussis toxin. Mice presented an initial acute phase characterized by accentuated weight loss and high clinical score, followed by a partial recovery when the animals reached normal body weight and smaller clinical scores. Spleen cells stimulated with MOG produced significantly higher levels of IFN- γ during the acute period whereas similar IL-17 levels were produced during both disease stages. CNS-infiltrating cells stimulated with MOG produced similar amounts of IFN- γ but, IL-17 was produced only at the acute phase of EAE. The percentage of Foxp3+ Treg cells, at the spleen and CNS, was elevated during both phases. The degree of inflammation was similar at both disease stages. Partial clinical recovery observed during chronic EAE was associated with no IL-17 production and presence of Foxp3+ Treg cells in the CNS.
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