Mice Encephalomyelitis in TCR BV 8 S 2 Transgenic Against Experimental Autoimmune TCR-Specific Regulation and Protection Vaccination with BV 8 S 2 Protein Amplifies

[1]  A. Vandenbark,et al.  Neonatal exposure of TCR BV8S2 transgenic mice to recombinant TCR BV8S2 results in reduced T cell proliferation and elevated antibody response to BV8S2, and increased severity of EAE , 1998, Journal of neuroscience research.

[2]  S. Tonegawa,et al.  Myelin Basic Protein–specific T Helper 2 (Th2) Cells Cause Experimental Autoimmune Encephalomyelitis in Immunodeficient Hosts Rather than Protect Them from the Disease , 1997, The Journal of experimental medicine.

[3]  H. D. Liggitt,et al.  Triggers of autoimmune disease in a murine TCR-transgenic model for multiple sclerosis. , 1997, Journal of immunology.

[4]  D. Bourdette,et al.  Treatment of multiple sclerosis with T–cell receptor peptides: Results of a double–blind pilot trial , 1996, Nature Medicine.

[5]  E. Sercarz,et al.  Dysregulation of potentially pathogenic self reactivity is crucial for the manifestation of clinical autoimmunity , 1996, Journal of neuroscience research.

[6]  D. Anthony,et al.  Immunization with T cell receptor V beta chain peptides deletes pathogenic T cells and prevents the induction of collagen-induced arthritis in mice. , 1996, The Journal of clinical investigation.

[7]  H. Offner,et al.  Natural immunodominant and experimental autoimmune encephalomyelitis‐protective determinants within the lewis rat Vβ8.2 sequence include CDR2 and framework 3 idiotopes , 1996, Journal of neuroscience research.

[8]  B. Ober,et al.  Self tolerance to T cell receptor V beta sequences , 1995, The Journal of experimental medicine.

[9]  T. Olsson.  Critical Influences of the Cytokine Orchestration on the Outcome of Myelin Antigen‐Specific T‐Cell Autoimmunity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis , 1995, Immunological reviews.

[10]  Laurie H Glimcher,et al.  B7-1 and B7-2 costimulatory molecules activate differentially the Th1/Th2 developmental pathways: Application to autoimmune disease therapy , 1995, Cell.

[11]  A. Vandenbark,et al.  Increased severity of experimental autoimmune encephalomyelitis in rats tolerized as adults but not neonatally to a protective TCR V beta 8 CDR2 idiotope. , 1995, Journal of immunology.

[12]  A. Weinberg,et al.  Coculture of TCR peptide-specific T cells with basic protein-specific T cells inhibits proliferation, IL-3 mRNA, and transfer of experimental autoimmune encephalomyelitis. , 1994, Journal of immunology.

[13]  E. Shevach,et al.  Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease. , 1994 .

[14]  Susumu Tonegawa,et al.  High incidence of spontaneous autoimmune encephalomyelitis in immunodeficient anti-myelin basic protein T cell receptor transgenic mice , 1994, Cell.

[15]  F. Finkelman,et al.  Effect of anti-interferon-γ monoclonal antibody treatment on the development of experimental allergic encephalomyelitis in resistant mouse strains , 1994, Journal of Neuroimmunology.

[16]  E. Sercarz,et al.  The involvement of T cell receptor peptide-specific regulatory CD4+ T cells in recovery from antigen-induced autoimmune disease , 1993, The Journal of experimental medicine.

[17]  A. Weinberg,et al.  Treatment of relapsing experimental autoimmune encephalomyelitis with T cell receptor peptides , 1993, Journal of neuroscience research.

[18]  L. Hood,et al.  Transgenic mice that express a myelin basic protein-specific T cell receptor develop spontaneous autoimmunity , 1993, Cell.

[19]  D. Bourdette,et al.  Myelin basic protein specific T cell lines and clones derived from the CNS of rats with EAE only recognize encephalitogenic epitopes , 1991, Journal of neuroscience research.

[20]  A. Vandenbark,et al.  T cell receptor peptide therapy triggers autoregulation of experimental encephalomyelitis. , 1991, Science.

[21]  B. Uitdehaag,et al.  Suppression of experimental allergic encephalomyelitis by intraventricular administration of interferon‐gamma in Lewis rats , 1990, Clinical and experimental immunology.

[22]  H. Offner,et al.  Antibodies specific for VB8 receptor peptide suppress experimental autoimmune encephalomyelitis. , 1990, Journal of immunology.

[23]  D. Carlo,et al.  Vaccination against experimental allergic encephalomyelitis with T cell receptor peptides. , 1989, Science.

[24]  A. Vandenbark,et al.  Immunization with a synthetic T-cell receptor V-region peptide protects against experimental autoimmune encephalomyelitis , 1989, Nature.

[25]  E. Heber-Katz,et al.  The V-region disease hypothesis: evidence from autoimmune encephalomyelitis. , 1989, Immunology today.

[26]  L. Hood,et al.  Restricted use of T cell receptor V genes in murine autoimmune encephalomyelitis raises possibilities for antibody therapy , 1988, Cell.

[27]  H. Mcdevitt,et al.  Limited heterogeneity of T cell receptors from lymphocytes mediating autoimmune encephalomyelitis allows specific immune intervention , 1988, Cell.

[28]  A. Billiau,et al.  Enhancement of experimental allergic encephalomyelitis in mice by antibodies against IFN-gamma. , 1988, Journal of immunology.

[29]  Lawrence Steinman,et al.  T-cell epitope of the autoantigen myelin basic protein that induces encephalomyelitis , 1986, Nature.

[30]  A. Vandenbark,et al.  Neonatal injection of Lewis rats with recombinant V beta 8.2 induces T cell but not B cell tolerance and increased severity of experimental autoimmune encephalomyelitis. , 1996, Journal of neuroscience research.

[31]  I. Cohen.  Resistance to Experimental Autoimmunity Using T Lymphocyte Vaccines , 1986 .

[32]  R. Martenson,et al.  Large scale preparation of myelin basic protein from central nervous tissue of several mammalian species. , 1972, Preparative biochemistry.