Peptidic complex mixtures as therapeutic agents in CNS autoimmunity.

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

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

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

[4]  R. Houghten General method for the rapid solid-phase synthesis of large numbers of peptides: specificity of antigen-antibody interaction at the level of individual amino acids. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[5]  L. Steinman,et al.  The T lymphocyte in experimental allergic encephalomyelitis. , 1990, Annual review of immunology.

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

[7]  H. Lassmann,et al.  Inflammation in the nervous system. Basic mechanisms and immunological concepts. , 1991, Revue neurologique.

[8]  J. Sidney,et al.  Single amino acid changes in DR and antigen define residues critical for peptide-MHC binding and T cell recognition. , 1991, Journal of immunology.

[9]  Eric O Long,et al.  A myelin basic protein peptide is recognized by cytotoxic T cells in the context of four HLA-DR types associated with multiple sclerosis , 1991, The Journal of experimental medicine.

[10]  D. McFarlin,et al.  Immunological aspects of demyelinating diseases. , 1992, Annual review of immunology.

[11]  Roland Martin,et al.  Copolymer-1-induced inhibition of antigen-specific T cell activation: interference with antigen presentation , 1992, Journal of Neuroimmunology.

[12]  C. Raine,et al.  Multiple sclerosis: immune system molecule expression in the central nervous system. , 1994, Journal of neuropathology and experimental neurology.

[13]  H. Rammensee,et al.  Ligand motifs of HLA-DRB5*0101 and DRB1*1501 molecules delineated from self-peptides. , 1994, Journal of immunology.

[14]  P. Allen Peptides in positive and negative selection: A delicate balance , 1994, Cell.

[15]  S. Tonegawa,et al.  A differential-avidity model for T-cell selection. , 1994, Immunology today.

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

[17]  A. Sette,et al.  Modulation of cytokine patterns of human autoreactive T cell clones by a single amino acid substitution of their peptide ligand. , 1995, Immunity.

[18]  V. Perry,et al.  Inflammation in the nervous system , 1995, Current Opinion in Neurobiology.

[19]  P. Allen,et al.  Essential flexibility in the T-cell recognition of antigen , 1996, Nature.

[20]  J. Haines,et al.  A complete genomic screen for multiple sclerosis underscores a role for the major histocompatability complex , 1996, Nature Genetics.

[21]  P. Goodfellow,et al.  A genome screen in multiple sclerosis reveals susceptibility loci on chromosome 6p21 and 17q22 , 1996, Nature Genetics.

[22]  P. Allen,et al.  Structural basis for T cell recognition of altered peptide ligands: a single T cell receptor can productively recognize a large continuum of related ligands , 1996, The Journal of experimental medicine.

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

[24]  M. Sela,et al.  Copolymer 1 inhibits chronic relapsing experimental allergic encephalomyelitis induced by proteolipid protein (PLP) peptides in mice and interferes with PLP-specific T cell responses , 1996, Journal of Neuroimmunology.

[25]  D. Hinds,et al.  A full genome search in multiple sclerosis , 1996, Nature Genetics.

[26]  R. Germain,et al.  Interleukin 2 production, not the pattern of early T-cell antigen receptor-dependent tyrosine phosphorylation, controls anergy induction by both agonists and partial agonists. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

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

[28]  R. Hohlfeld,et al.  Biotechnological agents for the immunotherapy of multiple sclerosis. Principles, problems and perspectives. , 1997, Brain : a journal of neurology.

[29]  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.

[30]  Bernhard Hemmer,et al.  Identification of High Potency Microbial and Self Ligands for a Human Autoreactive Class II–restricted T Cell Clone , 1997, The Journal of experimental medicine.

[31]  A. Sette,et al.  A T cell receptor antagonist peptide induces T cells that mediate bystander suppression and prevent autoimmune encephalomyelitis induced with multiple myelin antigens. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[32]  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.

[33]  Ariel Miller,et al.  Treatment of multiple sclerosis with Copolymer-1 (Copaxone®): implicating mechanisms of Th1 to Th2/Th3 immune-deviation , 1998, Journal of Neuroimmunology.

[34]  J. Whitaker,et al.  Current immunotherapy in multiple sclerosis , 1998, Immunology and cell biology.

[35]  M. Sela,et al.  Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1 , 1998, Journal of Neuroimmunology.

[36]  D. Mason,et al.  A very high level of crossreactivity is an essential feature of the T-cell receptor. , 1998, Immunology today.

[37]  R. Germain,et al.  The dynamics of T cell receptor signaling: complex orchestration and the key roles of tempo and cooperation. , 1999, Annual review of immunology.

[38]  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.

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

[40]  Clemencia Pinilla,et al.  Contribution of Individual Amino Acids Within MHC Molecule or Antigenic Peptide to TCR Ligand Potency1 , 2000, The Journal of Immunology.

[41]  C. Bever,et al.  Sustained clinical benefits of glatiramer acetate in relapsing multiple sclerosis patients observed for 6 years , 2000, Multiple Sclerosis.

[42]  G. Barger,et al.  Sustained clinical benefits of glatiramer acetate in relapsing multiple sclerosis patients observed for 6 years , 2000, Multiple sclerosis.

[43]  J. Frank,et al.  Encephalitogenic potential of the myelin basic protein peptide (amino acids 83–99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand , 2000, Nature Medicine.

[44]  C. Farina,et al.  Multiple sclerosis: comparison of copolymer-1- reactive T cell lines from treated and untreated subjects reveals cytokine shift from T helper 1 to T helper 2 cells. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[45]  A. Meshorer,et al.  Specific Th2 cells accumulate in the central nervous system of mice protected against experimental autoimmune encephalomyelitis by copolymer 1. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[46]  J. Antel,et al.  NBI‐5788, an altered MBP83‐99 peptide, induces a T‐helper 2–like immune response in multiple sclerosis patients , 2000, Annals of neurology.

[47]  R. Martin,et al.  Mechanisms of immunomodulation by glatiramer acetate , 2000, Neurology.

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

[49]  A. Evans,et al.  Induction of a non-encephalitogenic type 2 T helper-cell autoimmune response in multiple sclerosis after administration of an altered peptide ligand in a placebo-controlled, randomized phase II trial , 2000, Nature Medicine.

[50]  R. Martin,et al.  Glatiramer acetate induces a Th2-biased response and crossreactivity with myelin basic protein in patients with MS , 2001, Multiple sclerosis.

[51]  K. Garcia,et al.  Immunomodulation of Experimental Autoimmune Encephalomyelitis with Ordered Peptides Based on MHC-TCR Binding Motifs1 , 2001, The Journal of Immunology.

[52]  H. Rammensee,et al.  Ligand motif of the autoimmune disease‐associated mouse MHC class II molecule H2‐As , 2001, European journal of immunology.

[53]  C. Farina,et al.  Mechanisms of action of glatiramer acetate in multiple sclerosis , 2001, Neurology.

[54]  C. Brosnan,et al.  Novel synthetic amino acid copolymers that inhibit autoantigen-specific T cell responses and suppress experimental autoimmune encephalomyelitis. , 2002, The Journal of clinical investigation.