title: T cells that trigger acute experimental autoimmune encephalomyelitis also mediate subsequent disease relapses and predominantly produce IL-17.
abstract: Earlier studies showed that donor T cells that initiated a murine adoptive EAE persisted in the CNS of the recipients throughout the subsequent relapsing cycles. To clarify the functions of the persistent donor T cells in EAE relapsing disease, anti-Thy-1 antibodies were used to deplete these cells. Results showed that such treatment abrogated subsequent relapsing cycles in these animals. In addition, it was evident that a shift in cytokine profile occurred during acute and relapsing disease phases. These results unambiguously support the appropriateness of targeting T cells with specificity for the priming antigen in design of therapeutic approaches for MS.
authors.affiliation: Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
authors.forename: Jinzhu
authors.initials: J
authors.lastname: Li
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Zhao
authors.forename: Hui-Wen
authors.initials: HW
authors.lastname: Hao
authors.forename: Michael K
authors.initials: MK
authors.lastname: Shaw
authors.forename: Harley Y
authors.initials: HY
authors.lastname: Tse
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D002469:Cell Separation; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D020381:Interleukin-17 / Q000096:biosynthesis / Q000276:immunology*; D051379:Mice; D012008:Recurrence; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D018800:Thy-1 Antigens / Q000276:immunology / Q000378:metabolism
chemical_list: D020381:Interleukin-17; D018800:Thy-1 Antigens
references.citation: Nat Rev Immunol. 2002 Feb;2(2):85-95
references.pmid: 11910899
references.citation: Nature. 2003 Feb 13;421(6924):744-8
references.pmid: 12610626
references.citation: Curr Allergy Asthma Rep. 2003 Jan;3(1):86-93
references.pmid: 12543000
references.citation: Eur J Immunol. 1997 Nov;27(11):2927-34
references.pmid: 9394820
references.citation: J Neuroimmunol. 2005 Dec 30;170(1-2):105-14
references.pmid: 16257061
references.citation: J Immunol. 1998 Oct 15;161(8):4437-46
references.pmid: 9780223
references.citation: J Exp Med. 2008 Apr 14;205(4):799-810
references.pmid: 18391061
references.citation: J Exp Med. 1999 Apr 5;189(7):1033-42
references.pmid: 10190894
references.citation: J Autoimmun. 2000 Jun;14(4):278-82
references.pmid: 10882053
references.citation: J Immunol. 2000 Jan 15;164(2):670-8
references.pmid: 10623809
references.citation: Lab Invest. 1994 Nov;71(5):671-9
references.pmid: 7526038
references.citation: Mol Immunol. 2008 Feb;45(4):1191-6
references.pmid: 17697713
references.citation: Eur J Immunol. 1998 Dec;28(12):3893-903
references.pmid: 9862326
references.citation: J Exp Med. 1999 Apr 5;189(7):1021-4
references.pmid: 10190892
references.citation: J Exp Med. 1996 Apr 1;183(4):1777-88
references.pmid: 8666934
references.citation: Cell Immunol. 1985 Mar;91(1):240-54
references.pmid: 2578895
references.citation: J Neuroimmunol. 2007 Feb;183(1-2):96-103
references.pmid: 17240458
references.citation: Neurology. 1996 Apr;46(4):907-11
references.pmid: 8780061
references.citation: J Neurosci Res. 2007 Jun;85(8):1685-93
references.pmid: 17465017
references.citation: J Neuroimmunol. 1993 Jul;46(1-2):113-21
references.pmid: 7689581
references.citation: J Exp Med. 1995 Jul 1;182(1):75-85
references.pmid: 7540658
references.citation: J Neurosci Res. 1996 Sep 15;45(6):690-9
references.pmid: 8892080
references.citation: Nature. 1984 May 24-30;309(5966):356-8
references.pmid: 6203039
references.citation: J Immunol. 2009 Dec 1;183(11):7547-56
references.pmid: 19890052
references.citation: J Immunol. 2003 Feb 15;170(4):1690-8
references.pmid: 12574332
references.citation: J Neuroimmunol. 1993 Jul;46(1-2):129-36
references.pmid: 7689583