Persistent inflammation in the CNS during chronic EAE despite local absence of IL-17 production
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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. © 2013 Sofia Fernanda Gonçalves Zorzella-Pezavento et al.
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Freund adjuvant, gamma interferon, interleukin 17, myelin oligodendrocyte glycoprotein, pertussis toxin, transcription factor FOXP3, allergic encephalomyelitis, animal cell, animal experiment, animal model, body weight, cell infiltration, controlled study, cytokine production, disease severity, female, inflammatory infiltrate, mouse, nervous system inflammation, nonhuman, priority journal, regulatory T lymphocyte, scoring system, spleen cell, weight reduction
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English
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Mediators of Inflammation, v. 2013.






