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Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis.
Tohoku J Exp Med. 2007 Dec; 213(4):329-39.TJ

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-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). 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-gamma and TNF-alpha, 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.

Authors+Show Affiliations

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18075237

Citation

Sonobe, Yoshifumi, et al. "Chronological Changes of CD4(+) and CD8(+) T Cell Subsets in the Experimental Autoimmune Encephalomyelitis, a Mouse Model of Multiple Sclerosis." The Tohoku Journal of Experimental Medicine, vol. 213, no. 4, 2007, pp. 329-39.
Sonobe Y, Jin S, Wang J, et al. Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. Tohoku J Exp Med. 2007;213(4):329-39.
Sonobe, Y., Jin, S., Wang, J., Kawanokuchi, J., Takeuchi, H., Mizuno, T., & Suzumura, A. (2007). Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. The Tohoku Journal of Experimental Medicine, 213(4), 329-39.
Sonobe Y, et al. Chronological Changes of CD4(+) and CD8(+) T Cell Subsets in the Experimental Autoimmune Encephalomyelitis, a Mouse Model of Multiple Sclerosis. Tohoku J Exp Med. 2007;213(4):329-39. PubMed PMID: 18075237.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chronological changes of CD4(+) and CD8(+) T cell subsets in the experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. AU - Sonobe,Yoshifumi, AU - Jin,Shijie, AU - Wang,Jinyan, AU - Kawanokuchi,Jun, AU - Takeuchi,Hideyuki, AU - Mizuno,Tetsuya, AU - Suzumura,Akio, PY - 2007/12/14/pubmed PY - 2008/4/4/medline PY - 2007/12/14/entrez SP - 329 EP - 39 JF - The Tohoku journal of experimental medicine JO - Tohoku J. Exp. Med. VL - 213 IS - 4 N2 - 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-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). 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-gamma and TNF-alpha, 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. SN - 0040-8727 UR - https://www.unboundmedicine.com/medline/citation/18075237/Chronological_changes_of_CD4_+__and_CD8_+__T_cell_subsets_in_the_experimental_autoimmune_encephalomyelitis_a_mouse_model_of_multiple_sclerosis_ L2 - https://japanlinkcenter.org/JST.JSTAGE/tjem/213.329?lang=en&from=PubMed DB - PRIME DP - Unbound Medicine ER -