Glatiramer acetate induces a Th2-biased response and crossreactivity with myelin basic protein in patients with MS

Multiple Sclerosis

Volumn 7, Issue 4, 2001, Pages 209-219

  Chen, M ^a   Gran, B ^a   Costello, K ^a   Johnson, K ^a   Martin, R ^a   Dhib Jalbut, S ^a  

^a UNIVERSITY OF MARYLAND MEDICAL CENTER   (United States)

Author keywords

Copaxone ; Copolymer I; Glatiramer acetate; Immune deviation; Multiple sclerosis

Indexed keywords

ACETYLSALICYLIC ACID; ACICLOVIR; AMANTADINE; AMITRIPTYLINE; BACLOFEN; BETA1A INTERFERON; COTRIMOXAZOLE; CYTOKINE; FLAVOXATE; FLUOXETINE; FOSINOPRIL; GABAPENTIN; GAMMA INTERFERON; GLATIRAMER; GLIBENCLAMIDE; IBUPROFEN; INTERLEUKIN 5; MYELIN BASIC PROTEIN; PAROXETINE; PEPTIDE; PROPANTHELINE BROMIDE; SERTRALINE; TIZANIDINE;

ADULT; AGED; AMINO ACID SEQUENCE; ARTICLE; CELL LINE; CELLULAR IMMUNITY; CLINICAL ARTICLE; CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; CONTROLLED STUDY; CROSS REACTION; CYTOKINE RELEASE; DRUG APPROVAL; DRUG EXPOSURE; DRUG MECHANISM; DRUG SPECIFICITY; ENZYME LINKED IMMUNOSORBENT ASSAY; FEMALE; HUMAN; HUMAN CELL; IMMUNE RESPONSE; MALE; MEMBRANE MARKER; MULTIPLE SCLEROSIS; PROTEIN EXPRESSION; SUPERNATANT; T LYMPHOCYTE; TH1 CELL; TH2 CELL; TREATMENT OUTCOME;

CELL LINE; CROSS REACTIONS; CYTOKINES; ENZYME-LINKED IMMUNOSORBENT ASSAY; HUMANS; IMMUNOSUPPRESSIVE AGENTS; INTERLEUKIN-5; MULTIPLE SCLEROSIS; MYELIN BASIC PROTEINS; PEPTIDES; REGRESSION ANALYSIS; T-LYMPHOCYTES; TH2 CELLS;

EID: 0034882744     PISSN: 13524585     EISSN: None     Source Type: Journal    
DOI: 10.1191/135245801680209303     Document Type: Article

References (37)

1. Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide
2. Suppression of experimental allergic encephalomyelitis in Rhesus monkeys by a synthetic basic copolymer
3. Effect of treatment with Copolymer 1 (Cop-1) on the in vivo and in vitro manifestations of experimental allergic encephalomyelitis (EAE)
4. Copolymer 1 inhibits chronic relapsing experimental allergic encephalomyelitis induced by proteolipid protein (PLP) peptides in mice and interferes with PLP-specific T-cell responses
5. A pilot trial of COP 1 in exacerbating-remitting multiple sclerosis
6. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: Results of a phase III multicenter, double-blind, placebo-controlled trial
7. Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability. The Copolymer 1 Multiple Sclerosis Study Group
8. The effect of glatiramer acetate (Copaxone (R)) on disease activity as measured by cerebral MRI in patients with relapsing-remitting multiple sclerosis (RRMS): A multi-center, randomized, double blind, placebo-controlled study extended by open-label treatment
9. Direct binding of myelin basic protein and synthetic copolymer I to class II major histocompatibility complex molecules on living antigen-presenting cells - Specificity and promiscuity
10. Binding of copolymer 1 and myelin basic protein leads to clustering of class II MHC molecules on antigen-presenting cells
11. Promiscuous binding of synthetic copolymer 1 to purified HLA-DR molecules
12. Specific inhibition of the T-cell response to myelin basic protein by the synthetic copolymer Cop 1
13. Synthetic copolymer 1 inhibits human T-cell lines specific for myelin basic protein
14. The autoimmune reactivity to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis is potentially pathogenic: Effect of copolymer 1 on MOG-induced disease
15. 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
16. Mechanisms of immunomodulation by glatiramer acetate
17. Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis
18. T suppressor hybridomas and interleukin-2-dependent lines induced by copolymer 1 or by spinal cord homogenate down-regulate experimental allergic encephalomyelitis
19. Bystander suppression of experimental autoimmune encephalomyelitis by T-cell lines and clones of the Th2 type induced by copolymer 1
20. Treatment of multiple sclerosis with copolymer-1(Copaxone®): Implicating mechanism of Th1 to Th2/Th3 immune-deviation
21. Glatiramer acetate (Copaxone®) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosis
22. 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
23. Characterization of T-cell lines derived from glatiramer-acetate-treated multiple sclerosis patients
24. Mechanism of action of glatiramer acetate in multiple sclerosis
25. Antigen-driven bystander suppression after oral administration of antigens
26. 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
27. Diversity in fine specificity and T-cell receptor usage of the human CD4+ cytotoxic T-cell response specific for the immunodominant myelin basic protein peptide 87 - 106
28. Induction of Th1 and Th2 CD4+ T cell responses: The alternative approaches
29. Relationships among TCR ligand potency, thresholds for effector function elicitation, and the quality of early signaling events in human T cells
30. Oral tolerance with copolymer 1 for the treatment of multiple sclerosis
31. An altered peptide ligand mediates immune deviation and prevents autoimmune encephalomyelitis
32. Differential activation of human autoreactive T cell clones by altered peptide ligands derived from myelin basic protein peptide (87 - 99)
33. Modifications of peptide ligands enhancing T cell responsiveness imply large numbers of stimulatory ligands for autoreactive T cells
34. Immunogenic potentials of copolymer I in normal human lymphocytes
35. Human cellular immune response to copolymer I and myelin basic protein
36. Failure of copolymer I to inhibit the human T-cell response to myelin basic protein
37. Specific Th2 cells accumulate in the central nervous system of mice protected against experimental autoimmune encephalomyelitis by copolymer 1