Synthetic peptides that inhibit binding of the myelin basic protein 85-99 epitope to multiple sclerosis-associated HLA-DR2 molecules and MBP-specific T-cell responses.

[1]  R. Schiffer,et al.  Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability. 1998 [classical article]. , 2001, Neurology.

[2]  L. Fugger,et al.  Synthetic peptides that inhibit binding of the collagen type II 261-273 epitope to rheumatoid arthritis-associated HLA-DR1 and -DR4 molecules and collagen-specific T-cell responses. , 2000, Human immunology.

[3]  J. Krieger,et al.  Glatiramer acetate (Copaxone) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosis. , 2000, The Journal of clinical investigation.

[4]  L. Fugger,et al.  A humanized model for multiple sclerosis using HLA-DR2 and a human T-cell receptor , 1999, Nature Genetics.

[5]  J. Strominger,et al.  Binding of random copolymers of three amino acids to class II MHC molecules. , 1999, International immunology.

[6]  William Arbuthnot Sir Lane,et al.  Binding motifs of copolymer 1 to multiple sclerosis- and rheumatoid arthritis-associated HLA-DR molecules. , 1999, Journal of immunology.

[7]  M. Sela,et al.  Copolymer 1 acts against the immunodominant epitope 82-100 of myelin basic protein by T cell receptor antagonism in addition to major histocompatibility complex blocking. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[8]  Don C. Wiley,et al.  Crystal Structure of HLA-DR2 (DRA*0101, DRB1*1501) Complexed with a Peptide from Human Myelin Basic Protein , 1998, The Journal of experimental medicine.

[9]  L. Fugger,et al.  Synthetic amino acid copolymers that bind to HLA-DR proteins and inhibit type II collagen-reactive T cell clones. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[10]  J S Wolinsky,et al.  Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability , 1998, Neurology.

[11]  M. Fridkis-Hareli,et al.  Promiscuous binding of synthetic copolymer 1 to purified HLA-DR molecules , 1997, Journal of immunology.

[12]  A. Ben-nun,et al.  Predominance of the autoimmune response to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis: Reactivity to the extracellular domain of MOG is directed against three main regions , 1997, European journal of immunology.

[13]  M. Sela,et al.  Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[14]  J. Krieger,et al.  Changes in cytokine secretion induced by altered peptide ligands of myelin basic protein peptide 85-99. , 1997, Journal of immunology.

[15]  D. E. Anderson,et al.  Weak peptide agonists reveal functional differences in B7-1 and B7-2 costimulation of human T cell clones. , 1997, Journal of immunology.

[16]  A Sette,et al.  Complementary mutations in an antigenic peptide allow for crossreactivity of autoreactive T-cell clones. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[17]  J. Strominger,et al.  Expression of Recombinant HLA-DR2 Molecules , 1996, The Journal of Biological Chemistry.

[18]  U. Utz,et al.  Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein , 1996, Nature.

[19]  L. Weiner,et al.  Isolation and characterization of autoreactive moteolioid protein‐peptide specific T‐cell clones from multiple sclerosis patients , 1995, Neurology.

[20]  J. W. Rose,et al.  Copolymer 1 reduces relapse rate and improves disability in relapsing‐remitting multiple sclerosis , 1995, Neurology.

[21]  A. Waisman,et al.  Major T-cell responses in multiple sclerosis. , 1995, Molecular medicine today.

[22]  J. Strominger,et al.  Molecular mimicry in T cell-mediated autoimmunity: Viral peptides activate human T cell clones specific for myelin basic protein , 1995, Cell.

[23]  A. Sette,et al.  T cell recognition of immunodominant and cryptic proteolipid protein epitopes in humans , 1994, Journal of Neuroimmunology.

[24]  K. Parker,et al.  Autoreactive CD8+ cell responses to human myelin protein-derived peptides , 1994, Journal of Neuroimmunology.

[25]  D. Hafler,et al.  Clonal expansion and persistence of human T cells specific for an immunodominant myelin basic protein peptide. , 1994, Journal of immunology.

[26]  M. Sela,et al.  Direct binding of myelin basic protein and synthetic copolymer 1 to class II major histocompatibility complex molecules on living antigen-presenting cells--specificity and promiscuity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[27]  P. Travers,et al.  Modulation of the immune response with T-cell epitopes: the ultimate goal for specific immunotherapy of autoimmune disease. , 1994, Immunology.

[28]  Don C. Wiley,et al.  Crystal structure of the human class II MHC protein HLA-DR1 complexed with an influenza virus peptide , 1994, Nature.

[29]  H. Weiner,et al.  Increased frequency of interleukin 2-responsive T cells specific for myelin basic protein and proteolipid protein in peripheral blood and cerebrospinal fluid of patients with multiple sclerosis , 1994, The Journal of experimental medicine.

[30]  J. Hillert,et al.  The HLA-Dw2 haplotype segregates closely with multiple sclerosis in multiplex families , 1994, Journal of Neuroimmunology.

[31]  C Oseroff,et al.  Structural requirements for binding of an immunodominant myelin basic protein peptide to DR2 isotypes and for its recognition by human T cell clones , 1994, The Journal of experimental medicine.

[32]  A. Begovich,et al.  Genetic factors in multiple sclerosis. , 1993, JAMA.

[33]  L. Steinman,et al.  Induction of relapsing paralysis in experimental autoimmune encephalomyelitis by bacterial superantigen , 1993, Nature.

[34]  V. Gnau,et al.  Natural peptide ligand motifs of two HLA molecules associated with myasthenia gravis. , 1993, International immunology.

[35]  F. Sinigaglia,et al.  Promiscuous and allele-specific anchors in HLA-DR-binding peptides , 1993, Cell.

[36]  William Arbuthnot Sir Lane,et al.  Specificity and promiscuity among naturally processed peptides bound to HLA-DR alleles , 1993, The Journal of experimental medicine.

[37]  L. Adorini,et al.  Prevention of autoimmune diabetes in non-obese diabetic mice by treatment with a class II major histocompatibility complex-blocking peptide , 1993, The Journal of experimental medicine.

[38]  D. Eckels,et al.  Differential effect of polymorphism at HLA-DR1 beta-chain positions 85 and 86 on binding and recognition of DR1-restricted antigenic peptides. , 1993, Journal of immunology.

[39]  R. Arnon,et al.  T suppressor hybridomas and interleukin‐2‐dependent lines induced by copolymer 1 or by spinal cord homogenate down‐regulate experimental allergic encephalomyelitis , 1993, European journal of immunology.

[40]  F. Sinigaglia,et al.  Identification of a motif for HLA-DR1 binding peptides using M13 display libraries , 1992, The Journal of experimental medicine.

[41]  William S. Lane,et al.  Predominant naturally processed peptides bound to HLA-DR1 are derived from MHC-related molecules and are heterogeneous in size , 1992, Nature.

[42]  A. Rudensky,et al.  Sequence analysis of peptides bound to MHC class II molecules , 1991, Nature.

[43]  H. Weiner,et al.  T-cell recognition of myelin basic protein. , 1991, Immunology today.

[44]  H. Weiner,et al.  T-cell recognition of an immuno-dominant myelin basic protein epitope in multiple sclerosis , 1990, Nature.

[45]  R J Albertini,et al.  T cells responsive to myelin basic protein in patients with multiple sclerosis. , 1990, Science.

[46]  J. Rothbard,et al.  Prevention of experimental encephalomyelitis with peptides that block interaction of T cells with major histocompatibility complex proteins. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[47]  J. Todd,et al.  A molecular basis for MHC class II--associated autoimmunity. , 1988, Science.

[48]  S. Wassertheil-Smoller,et al.  A pilot trial of Cop 1 in exacerbating-remitting multiple sclerosis. , 1987, The New England journal of medicine.

[49]  R. Spielman,et al.  The genetics of susceptibility to multiple sclerosis. , 1982, Epidemiologic reviews.

[50]  A. Meshorer,et al.  Suppression of experimental allergic encephalomyelitis in Rhesus monkeys by a synthetic basic copolymer. , 1974, Clinical immunology and immunopathology.

[51]  A. Meshorer,et al.  Suppression by several synthetic polypeptides of experimental allergic encephalomyelitis induced in guinea pigs and rabbits with bovine and human basic encephalitogen , 1973, European journal of immunology.

[52]  A. Meshorer,et al.  Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide , 1971, European journal of immunology.