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1
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0028852336
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Spread of a neurotropic coronavirus to spinal cord white matter via neurons and astrocytes
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Sun N, Perlman S: Spread of a neurotropic coronavirus to spinal cord • white matter via neurons and astrocytes. J Virol 1995, 69:633-641. This study addressed the mechanism of virus spread from the brain to the spinal cord, suggesting transneuronal migration followed by cell-to-cell spread within the spinal cord through glial cells.
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Sun, N.1
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2
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0028795650
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Canine distemper virus persistence in the central nervous system is associated with non-cytolytic selective virus spread
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Zurbriggen A, Grabber HU, Wagner A, Vandevelde M: Canine distemper virus persistence in the central nervous system is associated with non-cytolytic selective virus spread. J Virol 1995, 69:1678-1686.
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3
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Studies on canine distemper virus persistence in the central nervous system
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Müller CF, Fatzer RS, Beck K, Vandevelde M, Zurbriggen A: Studies on canine distemper virus persistence in the central nervous system. Acta Neuropathol 1995, 89:438-445.
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Müller, C.F.1
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Zurbriggen, A.5
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4
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0029148439
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Persistent infection of cultured cells with mouse hepatitis virus (MHV) results from the epigenetic expression of the MHV receptor
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Sawicki SG, Lu J-H, Holmes KV: Persistent infection of cultured cells with mouse hepatitis virus (MHV) results from the epigenetic expression of the MHV receptor. J Virol 1995, 89:5535-5543.
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Sawicki, S.G.1
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5
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0028902180
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The predominant virus antigen burden is present in macrophages in Theller's murine encephalomyelitis virus-induced demyelinating disease
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Lipton HL, Twaddle G, Jelachich ML: The predominant virus antigen burden is present in macrophages in Theller's murine encephalomyelitis virus-induced demyelinating disease. J Virol 1995, 69:2525-2533.
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Lipton, H.L.1
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6
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0027273025
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Major role of antigen-presenting cells in the response of rat encephalitogenic T cells to myelin basic proteins
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Sun D, Le J, Yang S, Malostkey M, Coleclough C: Major role of antigen-presenting cells in the response of rat encephalitogenic T cells to myelin basic proteins. J Immunol 1993, 151:111-118.
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Sun, D.1
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7
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0027318299
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Diverse T cell receptor Vβ gene usage in the central nervous system in experimental allergic encephalomyelitis
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Bell R, Lindsey J, Sobel R, Hodgkinson S, Steinman L: Diverse T cell receptor Vβ gene usage in the central nervous system In experimental allergic encephalomyelitis. J Immunol 1993, 150:4085-4092.
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Bell, R.1
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8
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0029079491
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T lymphocyte repertoire in Theiler's virus encephalomyelitis: The nonspecific infiltration of the central nervous system of infected SJL/J mice is associated with selective local T cell expansion
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Musette P, Bureau J-F, Gachelin G, Kourilsky P, Brahic M: T lymphocyte • repertoire in Theiler's virus encephalomyelitis: the nonspecific infiltration of the central nervous system of infected SJL/J mice is associated with selective local T cell expansion. Eur J Immunol 1995, 25:1589-1593. Analysis of the TCR repertoire in the spinal cord of Theiler's virus-infected susceptible mice found all Vβ families, suggesting indiscriminate infiltration of T-cells in the CNS.
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Musette, P.1
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9
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0028672769
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Influence of deletion of T cell receptor Vβ genes on the Theiler's virus model of multiple sclerosis
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10
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0029036160
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T cell receptor (TCR) usage in lewis rat experimental autoimmune encephalomyelitis: TCR βchain-variable-region Vβ8.2-positive T cells are essential for induction and course of disease
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Gold R, Giegerich G, Hartung HP, Toyka KV: T cell receptor (TCR) • usage in lewis rat experimental autoimmune encephalomyelitis: TCR βchain-variable-region Vβ8.2-positive T cells are essential for induction and course of disease. Proc Natl Acad Sci USA 1995, 92: 5850-5854. Previous studies suggested that TCR β-chain gene Vβ8.2 dominates in MBP-induced EAE. In this study, EAE was induced using T-cells depleted of the Vβ89.2-positive fraction, indicating that this particular T-cells population is not essential for induction of EAE.
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Proc Natl Acad Sci USA
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Gold, R.1
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11
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0028888169
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Mouse hepatitis virus-specific cytotoxic T lymphocytes protect from lethal Infection without eliminating virus from the central nervous system
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Stohlman SA, Bergmann CC, van der Veen RC, Hinton DR: Mouse hepatitis virus-specific cytotoxic T lymphocytes protect from lethal Infection without eliminating virus from the central nervous system. J Virol 1995, 69:684-694.
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Stohlman, S.A.1
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12
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0028790908
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VP1 and VP2 capsid proteins of Theiler's virus are targets of H-2D-restricted cytotoxic lymphocytes in the central nervous system of B10 mice
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Lin X, Thiemann R, Pease LR, Rodriguez M: VP1 and VP2 capsid proteins • of Theiler's virus are targets of H-2D-restricted cytotoxic lymphocytes in the central nervous system of B10 mice. Virology 1995, 214:91-99. The experiments demonstrated H-2D but not H-2K-restricted Theiler's virus capsid proteins-specific cytotoxic T-cells in the CNS of infected mice. The fact that susceptibility to TMEV-induced demyelination maps to the same D region of MHC suggests preferential antigen presentation by H-2D over H-2K in this picornaviral infection.
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Lin, X.1
Thiemann, R.2
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0029258005
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d transgene suppresses Theiler's virus-induced demyelination in susceptible strains of mice
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d transgene suppresses Theiler's virus-induced demyelination In susceptible strains of mice. J Neurovirology 1995, 1:111-117.
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Rodriguez, M.1
David, C.S.2
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14
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0028931690
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Active and passively Induced experimental autoimmune encephalomyelitis in common marmosets: A new model for multiple sclerosis
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Massacesi L, Genain CP, Lee-Parritz D, Letvin NL, Canfield D, Hauser SL. • Active and passively Induced experimental autoimmune encephalomyelitis in common marmosets: a new model for multiple sclerosis. Ann Neurol 1995, 37:519-530. Reproducible EAE in primates should provide a useful model for analysis of immunopathologic mechanisms and therapeutic drugs.
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Ann Neurol
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Massacesi, L.1
Genain, C.P.2
Lee-Parritz, D.3
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Canfield, D.5
Hauser, S.L.6
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15
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0029129468
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Prevention of experimental allergic encephalomyelitis in rats by targeting autoantigen to B cells: Evidence that the protective mechanism depends on changes in the cytokine response and migratory properties of the autoantigen-specific T cells
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Saoudi A, Simmonds S, Huitinga I, Mason D: Prevention of experimental allergic encephalomyelitis in rats by targeting autoantigen to B cells: evidence that the protective mechanism depends on changes in the cytokine response and migratory properties of the autoantigen-specific T cells. J Exp Med 1995, 182:335-344.
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Saoudi, A.1
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16
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0029164864
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Mechanism of acquired thymic tolerance in experimental autoimmune encephalomyelitis: Thymic dendritic-enriched cells induce specific peripheral T cell unresponsiveness in vivo
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Khoury SJ, Gallon L, Chen W, Betres K, Russel ME, Hancock WW, •• Carpenter CB, Sayegh MF, Weiner HL: Mechanism of acquired thymic tolerance in experimental autoimmune encephalomyelitis: thymic dendritic-enriched cells induce specific peripheral T cell unresponsiveness in vivo. J Exp Med 1995, 182:357-366. This study investigated the mechanism of acquired thymic tolerance to MBP previously demonstrated to prevent induction of EAE. It suggests that the TCR of MBP-activated T-cells circulating through the thymus interact with thymic dendritic cells, leading to inactivation of these MBP-specific T-cells.
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J Exp Med
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Khoury, S.J.1
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17
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0029123992
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Exquisite peptlde specificity of oral tolerance in experimental autoimmune encephalomyelitis
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Javed NH, Gienapp IE, Cox KL, Whitacre CC: Exquisite peptlde specificity • of oral tolerance In experimental autoimmune encephalomyelitis. J Immunol 1995, 155:1599-1605. Lewis rats, treated orally with synthetic encephalitogenic MBP peptides GP 68-88 (from guinea pigs), but not with rat 68-88, were protected from EAE induced by both peptides. The two peptides differ by a single amino acid.
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J Immunol
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Javed, N.H.1
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18
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0029033375
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Reversal of acute experimental autoimmune encephalomyelitis and prevention of relapses by treatment with a myelin basic protein peptide analog modified to form long-lived peptide-MHC complexes
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Samson MF, Smilek DE: Reversal of acute experimental autoimmune • encephalomyelitis and prevention of relapses by treatment with a myelin basic protein peptide analog modified to form long-lived peptide-MHC complexes. J Immunol 1995, 155:2737-2746. More effective treatment of EAE was realized with a substitute MBP peptide that complexed with MHC molecules for a prolonged period, an important consideration for future therapeutic strategies of MS.
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J Immunol
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Samson, M.F.1
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19
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0029025863
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Tolerogenic forms of auto-antigens and cytokines in the induction of resistance to experimental allergic encephalomyelitis
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Santambragio L, Crisi GM, Leu J, Hochwald GM, Ryan T, Thorbecke GJ: Tolerogenic forms of auto-antigens and cytokines in the induction of resistance to experimental allergic encephalomyelitis. J Neuroimmunol 1995, 58:211-222.
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Santambragio, L.1
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Ryan, T.5
Thorbecke, G.J.6
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20
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0028796421
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Sequence 104-117 of myelin proteolipid protein is a cryptic encephalitogenic T cell determinant for SJL/J mice
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Tuohy VK, Thomas DM: Sequence 104-117 of myelin proteolipid protein is a cryptic encephalitogenic T cell determinant for SJL/J mice. J Neuroimmunol 1995, 56:161-170.
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J Neuroimmunol
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Tuohy, V.K.1
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21
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0029151449
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Experimental autoimmune peripheral neuritis Induced in BALB/c mice by myelin basic protein-specific T cell clones
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Abromson-Leeman S, Bronson R, Dorf ME: Experimental autoimmune • peripheral neuritis Induced in BALB/c mice by myelin basic protein-specific T cell clones. J Exp Med 1995, 182:587-592. As MS is exclusively a CNS disease, induction of peripheral nervous system demyelination by MBP-specific T-cells suggests that MBP is not the target antigen in MS.
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J Exp Med
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Abromson-Leeman, S.1
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22
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0029055672
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The proximal peripheral nervous system is a major site of demyelination in experimental autoimmune encephalomyelitis Induced in the Lewis rat by a myelin basic protein-specific T cells clone
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Pender MP, Tabi Z, Nguyen KB, McCombe PA: The proximal peripheral nervous system is a major site of demyelination In experimental autoimmune encephalomyelitis Induced in the Lewis rat by a myelin basic protein-specific T cells clone. Acta Neuropathol 1995, 89:527-531.
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Acta Neuropathol
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Pender, M.P.1
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23
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0029058504
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Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis
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Johns TG, de Rosbo NK, Menon KK, Abo S, Gonzales MF, Bernard CCA: Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis. J Immunol 1995, 154: 5536-5541.
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Johns, T.G.1
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24
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0029038922
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A myelin peptide Induces typical chronic experimental autoimmune encephalomyelitis in H-2b mice: Fine specificity and T cell receptor Vβ expression of encephalitogenic T cells
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Mendel I, de Rosbo NK, Ben-Nun A: A myelin peptide Induces typical • chronic experimental autoimmune encephalomyelitis in H-2b mice: fine specificity and T cell receptor Vβ expression of encephalitogenic T cells. Eur J Immunol 1995, 25:1951-1959. This study demonstrated induction of EAE by MOG peptide, pMOG 35-55, suggesting that MOG is a CNS autoantigen. This corroborated the finding of immune responses to MOG in patients with MS.
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Eur J Immunol
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Mendel, I.1
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25
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0028893387
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Over-expression of the DM-20 myelin proteolipid causes central nervous system demyelination in transgenic mice
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Johnson RS, Roder JC, Riordan JR: Over-expression of the DM-20 myelin proteolipid causes central nervous system demyelination In transgenic mice. J Neurochemistry 1995, 64:967-976.
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Johnson, R.S.1
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0029061716
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Theiler's virus Infection of 129Sv mice that lack the Interferon α/β or Interferon y receptors
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Fiette L, Aubert C, Müller U, Huang S, Aguet M, Brahic M, Bureau J-F: •• Theiler's virus Infection of 129Sv mice that lack the Interferon α/β or Interferon y receptors. J Exp Med 1995, 181:2069-2076. This study indicates that IFN-α/β is crucial for resistance to acute CNS virus infection, whereas IFN-γ plays a role in chronic infection but is not required for demyelination. IFN-α/β receptor-deficient mice developed acute fatal encephalitis after TMEV infection; IFN-γ receptor-deficient mice developed a persistent infection and more severe demyelination than that seen in susceptible non-mutant mice.
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J Exp Med
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Fiette, L.1
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Gamma Interferon is critical for resistance for Theiler's virus-induced demyelination
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Rodriguez M, Pavelko K, Coffman RL: Gamma Interferon Is critical for • resistance for Theiler's virus-induced demyelination. J Virol 1995, 69:7286-7290. These experiments demonstrated that treatment of mice with neutralizing antibodies to IFN-γ enhanced demyelination in susceptible mice and abrogated resistance in mice of resistant haplotype.
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Rodriguez, M.1
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Interferon Y, interleukin 4 and transforming growth factor βin experimental autoimmune encephalomyelitis in Lewis rats: Dynamics of cellular mRNA expression in the central nervous system and lymphoid cells
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Issazadeh S, Mustafa M, Ljundahl Å, Höjeberg B, Dagerlind Å, Elde R, Olsson T: Interferon Y, interleukin 4 and transforming growth factor βin experimental autoimmune encephalomyelitis in Lewis rats: dynamics of cellular mRNA expression in the central nervous system and lymphoid cells. J Neurosci Res 1995, 40:579-590.
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0028148199
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Reversal of experimental autoimmune encephalomyelitis by a soluble peptide variant of a myelin basic protein epitope: T cell receptor antagonism and reduction of Interferon y and tumor necrosis factor a production
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Karin N, Mitchell DJ, Brocke S, Ling N, Steinman L: Reversal of experimental autoimmune encephalomyelitis by a soluble peptide variant of a myelin basic protein epitope: T cell receptor antagonism and reduction of Interferon y and tumor necrosis factor a production. J Exp Med 1995, 180:2227-2237.
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Karin, N.1
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31
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0028903315
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Oral administration of human or murine Interferon alpha suppresses relapses and modifies adoptive transfer in experimental autoimmune encephalomyelitis
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Stohlman, S.A.1
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The receptor for tumor necrosis factor on murine astrocytes: Characterization, intracellular degradation, and regulation by cytokines and Theiler's murine encephalomyelitis virus
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Self and non-self peptides treat autoimmune encephalomyelitis: T cell anergy or competition for major hlstocompatibility complex class II binding?
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Gautman AM: Self and non-self peptides treat autoimmune encephalo• myelitis: T cell anergy or competition for major hlstocompatibility complex class II binding? Eur J Immunol 1995, 25:2059-2063. This study argues that peptide-induced tolerance is not a result of deletion or anergy of T-cells but the result of blocking MHC class II molecules.
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Insulin-like growth factor I treatment reduces demyelination and up-regulates gene expression of myelin-related proteins in experimental autoimmune encephalitis
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Yao D-L, Liu X, Hudson LD, Webster HD: Insulin-like growth factor I treat•• ment reduces demyelination and up-regulates gene expression of myelin-related proteins in experimental autoimmune encephalitis. Proc Natl Acad Sci USA 1995, 92:6190-6194. The findings indicate that IGF-1 can reduce the number and areas of demyelinating lesions by enhancing myelin protein synthesis and oligodendrocyte proliferation. This may be of major significance in future therapeutic strategies for demyelinating diseases.
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0029163665
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Differentiation of O-2A progenitor cell line CG-4 into oligodendrocytes and astrocytes following transplantation into glia-deficient areas of CNS white matter
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Franklin RJM, Bayley SA, Milner R, Ffrench-Constant C, Blakemore WF: •• Differentiation of O-2A progenitor cell line CG-4 into oligodendrocytes and astrocytes following transplantation into glia-deficient areas of CNS white matter. Glia 1995, 13:39-44. This study demonstrated remyelination after transplantation of a glial progenitor cell line. The cells differentiated into oligodendrocytes and astrocytes in vivo recreating the astrocyte-oligodendrocyte association which may be required for effective myelin production.
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45
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0029240387
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Glial cell transplants that are subsequently rejected can be used to influence regeneration of glial cell environments in the CNS
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Blakemore WF, Crang AJ, Franklin RJM, Tang K, Ryder S: Glial cell transplants that are subsequently rejected can be used to influence regeneration of glial cell environments in the CNS. Glia 1995, 13:79-91.
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46
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0028836830
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Glial-cell transplantation and plasticity in the O-2A lineage-implications for CNS repair
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Franklin RJM, Blakemore WF: Glial-cell transplantation and plasticity in the O-2A lineage-implications for CNS repair. Trends Neurosci 1995, 18:151-156.
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Monoclonal autoantibodies promote central nervous system repair in an animal model of multiple sclerosis
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Miller DJ, Sanbom KS, Katzmann JA, Rodriguez M: Monoclonal autoanti•• bodies promote central nervous system repair In an animal model of multiple sclerosis. J Neurosci 1994, 14:6230-6238. Two monoclonal autoantibodies, demonstrated subsequently to be natural autoantibodies [49], promoted CNS remyelination and reduced clinical deficits after virus-induced demyelination in mice. More recent investigation suggests that these autoantibodies act, at least in part, by suppressing CNS inflammation [50].
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Miller, D.J.1
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Miller DJ, Rodriguez M: Spontaneous and Induced remyelination in multiple sclerosis and the Theiler's virus model of central nervous system demyelination. Microscopy Res Tech 1995, 32:230-245.
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0028952443
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A monoclonal autoantlbody that promotes central nervous system remyelination in a model of multiple sclerosis is a natural autoantibody encoded by germline immunoglobulin genes
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Miller DJ, Rodnguez M: A monoclonal autoantlbody that promotes central nervous system remyelination in a model of multiple sclerosis Is a natural autoantibody encoded by germline immunoglobulin genes. J Immunol 1995, 154:2460-2469.
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A monoclonal natural autoantibody that promotes remyelination suppresses central nervous system Inflammation and Increases virus expression after Theiler's virus-induced demyelination
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Miller DJ, Njenga MK, Murray PD, Leibowitz J, Rodriguez M: A monoclonal natural autoantibody that promotes remyelination suppresses central nervous system Inflammation and Increases virus expression after Theiler's virus-induced demyelination. Int Immunol 1996, 8:131-141.
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0029057866
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Suppression of experimental autoimmune encephalomyelitis in Lewis rats by antibodies against CD2
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0028987311
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A monoclonal antibody to a4 integrin suppresses and reverses active experimental allergic encephalomyelitis
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Kent SJ, Karlik SJ, Cannon C, Hines DK, Yednock TA, Fritz LC, Homer HC: A • monoclonal antibody to a4 integrin suppresses and reverses active experimental allergic encephalomyelitis. J Neuroimmunol 1995, 58:1-10. This study demonstrates that prevention of leukocyte trafficking into the CNS, by blocking expression of a leukocyte adhesion molecule, can suppress clinical and pathologic features of EAE.
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53
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0029149732
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Antibodies against leukocyte function-associated antigen-1 and against intracellular adhesion molecule-1 together suppress the progression of experimental allergic encephalomyelitis
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Kobayashi Y, Kawai K, Honda H, Tomida S, Niimi N, Tamatani T, Miyasaka M, Yoshikai Y: Antibodies against leukocyte function-associated antigen-1 and against intracellular adhesion molecule-1 together suppress the progression of experimental allergic encephalomyelitis. Cellular Immunol 1995, 164:295-305.
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Racke MK, Bumett D, Pak S-H, Albert PS, Cannella B, Raine CS, McFarlin DE, Scott DE: Retinoid treatment of experimental allergic encephalomyelitis. IL-4 production correlates with Improved disease course. J Immunol 1995, 154:450-458.
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