Chronological Changes of CD4+ and CD8+ T Cell Subsets in the Experimental Autoimmune Encephalomyelitis, a Mouse Model of Multiple Sclerosis
Open Access
- 1 January 2007
- journal article
- Published by Tohoku University Medical Press in The Tohoku Journal of Experimental Medicine
- Vol. 213 (4), 329-339
- https://doi.org/10.1620/tjem.213.329
Abstract
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS). The etiology of MS remains unclear, but T cells specific for myelin components, such as myelin oligodendrocyte glycoprotein (MOG), are thought to play a critical role in the onset of MS. Experimental autoimmune encephalomyelitis (EAE) has been used as an animal model of MS, and T helper type 1 (Th1) cells play an essential role for the pathogenesis of EAE through the production of Th1 cytokines, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). We examined CD4+ and CD8+ T cell responses in the spleen and CNS of EAE mice, generated by immunization with a peptide (35-55 amino acid residues) of MOG. The number of both CD4+ and CD8+ T cells and their MOG-reactivity in the CNS were associated with increasing disease severity but not those in the spleen, suggesting that the MOG-specific CD4+ and CD8+ T cells in the CNS are involved in the development of EAE. Polymerase chain reaction analysis suggested that both CD4+ and CD8+ T cells produced IFN-γ and TNF-α, while CD4+ T cells also produced interleukin-17 (IL-17), an important factor in the development of EAE. Thus, CD4+ T cells may contribute to the induction of EAE by producing IL-17. Furthermore, CD8+ T cells express higher levels of a suppressive cytokine, IL-10. Taking together, our data suggest that CD4+ T cells are involved in the early phase of EAE, whereas CD8+ T cells have a regulatory role in the later stage of EAE.Keywords
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