Mechanisms of immunomodulation by glatiramer acetate

Neurology

Volumn 55, Issue 11, 2000, Pages 1704-1714

  Gran, B ^a   Tranquill, L R ^a   Chen, M ^b   Bielekova, B ^a   Zhou, W ^a   Dhib Jalbut, S ^b   Martin, Roland ^a  

^a NATIONAL INSTITUTES OF HEALTH   (United States)

^b UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BACTERIAL ANTIGEN; CYTOKINE; GLATIRAMER; HLA ANTIGEN; INFLUENZA VIRUS HEMAGGLUTININ; MYELIN BASIC PROTEIN; T LYMPHOCYTE RECEPTOR;

ADULT; ARTICLE; BORRELIA BURGDORFERI; CASE REPORT; CLONAL ANERGY; CONTROLLED STUDY; CYTOKINE RELEASE; DRUG MECHANISM; FEMALE; HUMAN; HUMAN CELL; IMMUNOMODULATION; INFLUENZA VIRUS; MALE; MULTIPLE SCLEROSIS; PRIORITY JOURNAL; RECEPTOR DOWN REGULATION; T LYMPHOCYTE ACTIVATION; TH1 CELL; TH2 CELL;

EID: 0034642206     PISSN: 00283878     EISSN: None     Source Type: Journal    
DOI: 10.1212/WNL.55.11.1704     Document Type: Article

References (40)

1. A pilot trial of COP 1 in exacerbating-remitting multiple sclerosis
2. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: Results of a phase III multicenter, double-blind, placebo-controlled trial
3. Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability
4. The effect of glatiramer acetate (Copaxone) on disease activity as measured by cerebral MRI in patients with relapsing-remitting multiple sclerosis (RRMS): A multicenter, randomized, double blind, placebo-controlled study extended by open-label treatment
5. Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide
6. Suppression of experimental allergic encephalomyelitis in Rhesus monkeys by a synthetic basic copolymer
7. Effect of treatment with Copolymer 1 (Cop-1) on the in vivo and in vitro manifestations of experimental allergic encephalomyelitis (EAE)
8. Copolymer 1 inhibits chronic relapsing experimental allergic encephalomyelitis induced by proteolipid protein (PLP) peptides in mice and interferes with PLP-specific T cell responses
9. Specific inhibition of the T-cell response to myelin basic protein by the synthetic copolymer Cop 1
10. Synthetic copolymer 1 inhibits human T-cell lines specific for myelin basic protein
11. The autoimmune reactivity to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis is potentially pathogenic: Effect of copolymer 1 on MOG-induced disease
12. 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
13. Binding of copolymer 1 and myelin basic protein leads to clustering of class II MHC molecules on antigen-presenting cells
14. Promiscuous binding of synthetic copolymer 1 to purified HLA-DR molecules
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. Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis
17. T suppressor hybridomas and interleukin-2-dependent lines induced by copolymer 1 or by spinal cord homogenate downregulate experimental allergic encephalomyelitis
18. Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1
19. Antigen-driven bystander suppression after oral administration of antigens
20. General method for the rapid solid-phase synthesis of large numbers of peptides: Specificity of antigenantibody interaction at the level of individual amino acids
21. A myelin basic protein peptide is recognized by cytotoxic T cells in the context of four HLA-DR types associated with multiple sclerosis
22. 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
23. Differential activation of human autoreactive T cell clones by altered peptide ligands derived from myelin basic protein peptide (87-99)
24. Modifications of peptide ligands enhancing T cell responsiveness imply large numbers of stimulatory ligands for autoreactive T cells
25. Immunodominance of a low-affinity major histocompatibility complex-binding myelin basic protein epitope (residues 111-129) in HLA-DR4 (B1*0401) subjects is associated with a restricted T cell receptor repertoire
26. Antigen analogs/MHC complexes as specific T cell receptor antagonists
27. Antigen analog-major histocompatibility complexes act as antagonists of the T-cell receptor
28. Induction of T-cell anergy by altered T-cell-receptor ligand on live antigen-presenting cells
29. Cytokine phenotype of human autoreactive T cell clones specific for the immunodominant myelin basic protein peptide (83-99)
30. Preferential expansion of autoreactive T lymphocytes from the memory T-cell pool by IL-7
31. Failure of copolymer I to inhibit the human T-cell response to myelin basic protein
32. Relationships among TCR ligand potency, thresholds for effector function elicitation, and the quality of early signaling events in human T cells
33. Glatiramer acetate (Copaxone) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosis
34. Oral tolerance with copolymer 1 for the treatment of multiple sclerosis
35. An altered peptide ligand mediates immune deviation and prevents autoimmune encephalomyelitis
36. Immunogenic potentials of copolymer I in normal human lymphocytes
37. Human cellular immune response to copolymer I and myelin basic protein
38. Repertoire breadth of human CD4+ T cells specific for HIV gp120 and p66 (primary antigens) or for PPD and tetanus toxoid (secondary antigens)
39. T-cell signaling: The importance of receptor clustering
40. Induction of Th1 and Th2 CD4+ T cell responses: The alternative approaches