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- W2177571306 abstract "Abstract Multiple sclerosis (MS) is a progressive demyelinating disease associated with chronic inflammation in the central nervous system (CNS). Genetic linkage is found in genes related to T cell function, and T cell infiltration is evident in MS lesions, suggesting a pathophysiological role for these cells. In the MS animal model experimental autoimmune encephalomyelitis (EAE), activated CD4+ and CD8+ T cells that recognize CNS antigens can induce MS-like symptoms. Various cytokines from these T cells trigger inflammation, critically contributing to the pathogenesis of the CNS disease. Evidence suggests an important role for cytokine-mediated crosstalk between T cells and nonimmune cells, including endothelial cells, glial cells, and fibroblasts in enhancing CNS inflammation. Counterbalancing T cell-induced inflammation, certain regulatory CD4+ and CD8+ T cell subsets can suppress CNS disease progression. Here, we discuss the pathophysiological role of T cells during MS and EAE, including neuro–immune interactions that allow T cells to invade the CNS." @default.
- W2177571306 created "2016-06-24" @default.
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- W2177571306 date "2016-01-01" @default.
- W2177571306 modified "2023-10-02" @default.
- W2177571306 title "Role of Cytokine-Mediated Crosstalk between T Cells and Nonimmune Cells in the Pathophysiology of Multiple Sclerosis" @default.
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