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1
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0029072403
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Genes and susceptibility to multiple sclerosis
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Compston DAS, Kellar Wood H, Robertson M, Sawcer S, Wood NW: • Genes and susceptibility to multiple sclerosis. Acta Neurol Scand 1995, 161(suppl):43-51. Comprehensive and current literature review on genes and susceptibility to MS.
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Acta Neurol Scand
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Compston, D.A.S.1
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2
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0029142819
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Plaque-associated expression of human herpesvlrus 6 in multiple sclerosis
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Challoner PB, Smith KT, Parker JD, Macleod DL, Coulter SN, Rose TM, • Schultz ER, Bennett JL, Garber RL, Chang M et al.: Plaque-associated expression of human herpesvlrus 6 in multiple sclerosis. Proc Natl Acad Sci U S A 1995, 92:7440-7444. Exciting discovery of a possible aetiological role of HHV-6 in MS.
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3
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0028869486
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The basis of autoimmunity. Part I. Mechanisms of aberrant self-recognition
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Theofilopoulos AN: The basis of autoimmunity. Part I. Mechanisms of aberrant self-recognition. Immunol Today 1995, 16:90-98.
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Theofilopoulos, A.N.1
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Molecular mimicry in T cell-mediated autoimmunity: Viral peptides activate human T cell clones specific for myeline basic protein
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Wucherpfennig KW, Strominger JL: Molecular mimicry in T cell-mediated •• autoimmunity: viral peptides activate human T cell clones specific for myeline basic protein. Cell 1995, 80:695-705. These authors identified peptide motifs required for MHC class II binding and TCR recognition of the immunodominant MBP(85-99) peptide. These were comparable with a protein database for viral and bacterial pathogens that could be relevant to inflammatory disease of the central nervous system. MBP(85-99). specific T-cell clones could be activated by mimicry peptides of herpes simplex, Epstein-Barr virus, adenovirus 12, influenza type A and Pseudomonas aeruginosa. Viral mimicry peptides were more effectively presented by MS-associated DR2 molecules. Activation of MBP-specific T-cells by viral peptides would constitue a mechanism by which autoimmune responses are triggered in MS.
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Cell
, vol.80
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Wucherpfennig, K.W.1
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B7-1 and B7-2 co-stimulatory molecules activate differentially the Th-1/Th-2 developmental pathways: Application to autoimmune disease therapy
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Kuchroo VK, Das MP, Brown JA, Ranger AM, Zamvil SS, Sobel RA, •• Weiner HL, Nabavi N, Glimcher LH: B7-1 and B7-2 co-stimulatory molecules activate differentially the Th-1/Th-2 developmental pathways: application to autoimmune disease therapy. Cell 1995, 80:707-718. Very important findings documenting the different T-helper developmental pathways and the potential therapeutic implications from manipulating their development.
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Kuchroo, V.K.1
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6
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0028999041
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Long-term Inhibition of murine experimental autoimmune encephalomyelitis using CTLA-4-Fc supports a key role for CD28 co-stimulation
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Cross AH, Girard TJ, Giacoletto KS, Evans RJ, Keeling RM, Lin RF, Trotter JL, Karr RW: Long-term Inhibition of murine experimental autoimmune encephalomyelitis using CTLA-4-Fc supports a key role for CD28 co-stimulation. J Clin Invest 1995, 95:2783-2789.
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7
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Distinct roles for B7-1 (CD80) and B7-2 (CD-86) in the initiation of experimental allergic encephalomyelitls
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Racke MK, Scott DE, Quigley L, Gray GS, Abe R, June CH, Perrin PJ: Distinct roles for B7-1 (CD80) and B7-2 (CD-86) in the initiation of experimental allergic encephalomyelitls. J Clin Invest 1995, 96:2195-2203.
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8
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0028964455
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The co-stimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions
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De Simone R, Giampaolo A, Gallo P, Levi G, Peschle C, Aloisi F: The co-stimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions. J Neuropathol Exp Neurol 1995, 50:175-187.
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9
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0029314934
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The role of autoimmune T lymphocytes in the pathogenesis of multiple sclerosis
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Hohlfeld R, Meinl E, Weber F, Zipp F, Schmidt S, Sotigiu S, Goebels N, Voltz R, Spuler S, Iglesias A, Wekerle H: The role of autoimmune T lymphocytes in the pathogenesis of multiple sclerosis. Neurology 1995, 45(suppl 6):S33-S38.
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Hohlfeld, R.1
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Immunological aspects of experimental allergic encephalomyelitls and multiple sclerosis
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Martin R, McFarland HF: Immunological aspects of experimental allergic •• encephalomyelitls and multiple sclerosis. Crit Rev Clin Lab Sci 1995, 32:121-182. An excellent authoritative review with 384 references.
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Martin, R.1
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0028053609
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Lodge PA, Allegretta M, Steinman L, Subramaniam S: Myelin basic protein specficlty and T-cell receptor gene usage of HPRT mutant T-cell clones in patients with multiple sclerosis. Ann Neurol 1994, 36:734-740.
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Increased frequencles of HPRT mutant T lymphocytes in patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy: Further evidence for a role of T cells in the etiopathogenesis of peripheral demyelinating diseases
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van den Berg LH, Mollee I, Wokke JH, Logtenberg T: Increased frequencles of HPRT mutant T lymphocytes in patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy: further evidence for a role of T cells in the etiopathogenesis of peripheral demyelinating diseases. J Neuroimmunol 1995, 58:37-42.
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Selection for T-cell receptor Vβ-Dβ-Jβ gene rearrangements with specificity for myelin basic protein peptide in brain lesions of multiple sclerosis
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Oksenberg JR, Panzara MA, Begovich AB, Mitchell D, Erlich HA, Murray RS, Shimonkevitz R, Sherritt M, Rothbard J, Bernard CCA, Steinman L: Selection for T-cell receptor Vβ-Dβ-Jβ gene rearrangements with specificity for myelin basic protein peptide in brain lesions of multiple sclerosis. Nature 1993, 362:68-70
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Characteristics of the T lymphocytes involved in experimental allergic encephalomyelitls
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Kalman B, Alder H, Lublin FD: Characteristics of the T lymphocytes involved in experimental allergic encephalomyelitls. J Neuroimmunol 1995, 61:107-116.
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0030069166
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TCR repertoire to proteolipid protein (PLP) in multiple sclerosis (MS): Homologies between PLP-specific T cells and MS-associated T cells in TCR junctional sequences
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Kondo T, Yamamura T, Inobe J, Ohashi T, Takahashi K, Tabira T: TCR repertoire to proteolipid protein (PLP) in multiple sclerosis (MS): homologies between PLP-specific T cells and MS-associated T cells in TCR junctional sequences. Int Immunol 1996, 8:123-130.
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A review of T-cell receptors in multiple sclerosis: Clonal expansion an persistence of human T-cells specific for an immunodominant myelin basic protein peptide
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Allegretta M, Steinman L: Unique T-cell receptor junctional sequences found in multiple sclerosis and T-cells mediating experimental allergic encephalomyelitls. Ann NY Acad Sci 1995, 756:265-282.
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T-cell receptor use in multiple sclerosis
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Linington C, Waksman B: The T-cell receptor in multiple sclerosis. Ann N Y Acad Sci 1995, 756:294-306.
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Ann N Y Acad Sci
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20
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0029036160
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T-cell receptor (TCR) usage in Lewis rat experimental autoimmune encephalomyelitis: TCR β-chain-variable-region Vβ8.2-positive T cells are not essential for induction and course of disease
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Gold R, Giegerich G, Hatrung H-P, Toyka KV: T-cell receptor (TCR) usage in Lewis rat experimental autoimmune encephalomyelitis: TCR β-chain-variable-region Vβ8.2-positive T cells are not essential for induction and course of disease. Proc Natl Acad Sci U S A 1995, 92: 5850-5854.
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Gold, R.1
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Decreased CD3-mediated interferon-γ production in relapsing-remitting multiple sclerosis
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Brod SA, Khan M, Bright J, Sriram S, Marshall GD, Henninger EM, Kerman RH, Wolinsky JS: Decreased CD3-mediated interferon-γ production in relapsing-remitting multiple sclerosis. Ann Neurol 1995, 37:546-549.
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Reduced expression of peptide-loaded HLA class I molecules on multiple sclerosis lymphocytes
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Li F, Linan MJ, Stein MC, Faustman DL: Reduced expression of peptide-loaded HLA class I molecules on multiple sclerosis lymphocytes. Ann Neurol 1995, 38:147-154.
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Circulating natural killer cells but not cytotoxic T lymphocytes are reduced in patients with active relapsing multiple sclerosis and little clinical disability as compared to controls
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Munschaur FE, Hartrich LA, Stewart CC, Jacobs L: Circulating natural killer cells but not cytotoxic T lymphocytes are reduced in patients with active relapsing multiple sclerosis and little clinical disability as compared to controls. J Neuroimmunol 1995, 62:177-181.
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