2001
DOI: 10.1006/jaut.2001.0520
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Role of MOG-stimulated Th1 type ‘light up’ (GFP+) CD4+T Cells for the Development of Experimental Autoimmune Encephalomyelitis (EAE)

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Cited by 48 publications
(31 citation statements)
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“…This effect may block IFN-γ-mediated Th17 immune responses in EAE mice and inhibit EAE development. Moreover, IFN-γ is produced by Th1 cells, which also play an important role in EAE induction [60]. Our ELISA data demonstrated that LPS-treated DCs down-regulate the amount of IFN-γ, suggesting that LPStreated DCs may also affect the activity of Th1 cells via down-regulation of IFN-γ production.…”
Section: B220mentioning
confidence: 60%
“…This effect may block IFN-γ-mediated Th17 immune responses in EAE mice and inhibit EAE development. Moreover, IFN-γ is produced by Th1 cells, which also play an important role in EAE induction [60]. Our ELISA data demonstrated that LPS-treated DCs down-regulate the amount of IFN-γ, suggesting that LPStreated DCs may also affect the activity of Th1 cells via down-regulation of IFN-γ production.…”
Section: B220mentioning
confidence: 60%
“…The first cell type we examined was the CD4 ϩ T cell, which is responsible for mediating EAE. 21,22 Since previous work had shown that TIMP-1 can be expressed by CD4 ϩ T cells, 23 we considered that the absence of TIMP-1 may have altered the development or magnitude of a myelin-specific CD4 ϩ T-cell response in MOG 35-55 -immunized mice. To test this, we isolated and pooled the cellular infiltrates from spinal cords of WT and TIMP-1 Ϫ/Ϫ mice, either acute phase (18 days) or chronic phase (52 days), after immunization with MOG and used flow cytometry to identify and quantify the antigen-specific T-cell response, using peptide-stimulated IFN-␥ production as a marker of activation.…”
Section: Cd4 ϩ T-cell Responses During Eaementioning
confidence: 99%
“…Among CD4 + T cells, the T helper 1 cell subpopulation has been distinctively attributed a major role in the promotion of EAE (Yura et al 2001). Pathogenic properties of Th1 are mediated by highly pro-inflammatory and cytotoxic cytokines, such as interferongamma (IFN-g) (Bradley et al 1996;Xiao et al 2008) and tumor necrosis factor-alpha (TNF-a) (Selmaj and Raine 1988).…”
Section: Article In Pressmentioning
confidence: 99%
“…EAE is primarily mediated by CD4 + T cells specific for autoantigens in the CNS (Brostoff and Mason 1984;Yura et al 2001). During the induction phase of EAE, activated proinflammatory CD4 + T cells proliferate in the periphery and infiltrate the central nervous system (CNS) through interaction with endothelial cells, which facilitate the blood-brain barrier crossing (Cassan and Liblau 2007).…”
Section: Article In Pressmentioning
confidence: 99%