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PMID: 10861010 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

T cell immunity to copolymer 1 confers neuroprotection on the damaged optic nerve: possible therapy for optic neuropathies.

Kipnis J, Yoles E, Porat Z, Cohen A, Mor F, Sela M, Cohen IR, Schwartz M

Abstract

We recently reported that the posttraumatic spread of degeneration in the damaged optic nerve can be attenuated by the adoptive transfer of autoimmune T cells specific to myelin basic protein. However, it would be desirable to obtain immune neuroprotection free of any possible autoimmune disease. In an attempt to obtain disease-free immune neuroprotection, we used the synthetic four-amino acid polymer copolymer 1 (Cop-1), which is known not to be encephalitogenic despite its cross-reactivity with myelin basic protein. We show here that active immunization with Cop-1 administered in adjuvant, as well as adoptive transfer of T cells reactive to Cop-1, can inhibit the progression of secondary degeneration after crush injury of the rat optic nerve. These results have implications for the treatment of optic neuropathies.

MeSH Terms
Animals Antigen Presentation Female Glatiramer Acetate Immunity, Cellular Immunotherapy, Adoptive Optic Nerve/immunology,pathology Optic Nerve Diseases/immunology,therapy Peptides/administration & dosage,immunology Rats Rats, Inbred Lew T-Lymphocytes/immunology
Chemicals
Peptides Glatiramer Acetate
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Kipnis J
Departments of Neurobiology and Immunology, The Weizmann Institute of Science, 76100 Rehovot, Israel.
Yoles E
Porat Z
Cohen A
Mor F
Sela M
Cohen I R
Schwartz M
References (33)
33 references, click to expand
  1. Oral tolerance for the treatment of autoimmune diseases.
    Annu Rev Med. 1997;48:341-51 PMID: 9046967
  2. A monoclonal antibody to a constant determinant of the rat T cell antigen receptor that induces T cell activation. Differential reactivity with subsets of immature and mature T lymphocytes.
    J Exp Med. 1989 Jan 1;169(1):73-86 PMID: 2783336
  3. Binding of random copolymers of three amino acids to class II MHC molecules.
    Int Immunol. 1999 May;11(5):635-41 PMID: 10330269
  4. Potential neuroprotective therapy for glaucomatous optic neuropathy.
    Surv Ophthalmol. 1998 Jan-Feb;42(4):367-72 PMID: 9493279
  5. T cell growth factor: parameters of production and a quantitative microassay for activity.
    J Immunol. 1978 Jun;120(6):2027-32 PMID: 307029
  6. Autoimmune T cells as potential neuroprotective therapy for spinal cord injury.
    Lancet. 2000 Jan 22;355(9200):286-7 PMID: 10675079
  7. Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide.
    Eur J Immunol. 1971 Aug;1(4):242-8 PMID: 5157960
  8. Neuroprotection: a new treatment modality for glaucoma?
    Curr Opin Ophthalmol. 2000 Apr;11(2):107-11 PMID: 10848215
  9. Diagnosis and pathogenesis of glaucomatous optic neuropathy: morphological aspects.
    Prog Retin Eye Res. 2000 Jan;19(1):1-40 PMID: 10614679
  10. T-lymphocyte entry into the central nervous system.
    J Neurosci Res. 1991 Feb;28(2):254-60 PMID: 2033653
  11. Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation?
    J Exp Med. 1999 Mar 1;189(5):865-70 PMID: 10049950
  12. T suppressor hybridomas and interleukin-2-dependent lines induced by copolymer 1 or by spinal cord homogenate down-regulate experimental allergic encephalomyelitis.
    Eur J Immunol. 1993 Jan;23(1):17-25 PMID: 8419168
  13. Differential T cell response in central and peripheral nerve injury: connection with immune privilege.
    FASEB J. 1999 Jul;13(10):1207-17 PMID: 10385611
  14. The rapid isolation of clonable antigen-specific T lymphocyte lines capable of mediating autoimmune encephalomyelitis.
    Eur J Immunol. 1981 Mar;11(3):195-9 PMID: 6165588
  15. Degeneration of spared axons following partial white matter lesion: implications for optic nerve neuropathies.
    Exp Neurol. 1998 Sep;153(1):1-7 PMID: 9743562
  16. Traumatic optic neuropathy.
    Curr Opin Ophthalmol. 1999 Oct;10(5):340-2 PMID: 10621549
  17. Copolymer 1 from the laboratory to FDA.
    Isr J Med Sci. 1997 Apr;33(4):280-4 PMID: 9347880
  18. Graded crush of the rat optic nerve as a brain injury model: combining electrophysiological and behavioral outcome.
    Restor Neurol Neurosci. 1990 Jan 1;2(1):31-8 PMID: 21551870
  19. Copolymer 1 inhibits chronic relapsing experimental allergic encephalomyelitis induced by proteolipid protein (PLP) peptides in mice and interferes with PLP-specific T cell responses.
    J Neuroimmunol. 1996 Feb;64(2):209-17 PMID: 8632064
  20. Correlation between strain differences in susceptibility to experimental allergic encephalomyelitis and the immune response to encephalitogenic protein in inbred guinea pigs.
    Immunol Commun. 1973;2(2):185-92 PMID: 4726657
  21. Self-destructive and self-protective processes in the damaged optic nerve: implications for glaucoma.
    Invest Ophthalmol Vis Sci. 2000 Feb;41(2):349-51 PMID: 10670461
  22. Specific inhibition of the T-cell response to myelin basic protein by the synthetic copolymer Cop 1.
    Proc Natl Acad Sci U S A. 1988 Dec;85(24):9724-8 PMID: 2462252
  23. The autoimmune reactivity to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis is potentially pathogenic: effect of copolymer 1 on MOG-induced disease.
    J Neurol. 1996 Apr;243(4 Suppl 1):S14-22 PMID: 8965116
  24. Innate and adaptive immune responses can be beneficial for CNS repair.
    Trends Neurosci. 1999 Jul;22(7):295-9 PMID: 10370250
  25. Oral tolerance: immune mechanisms and treatment of autoimmune diseases.
    Immunol Today. 1997 Jul;18(7):335-43 PMID: 9238837
  26. Experimental autoimmune encephalomyelitis (EAE) mediated by T cell lines: process of selection of lines and characterization of the cells.
    J Immunol. 1982 Jul;129(1):303-8 PMID: 6177753
  27. Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis.
    Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10821-6 PMID: 9380718
  28. Brain-derived neurotrophic factor prevents the death of motoneurons in newborn rats after nerve section.
    Nature. 1992 Dec 24-31;360(6406):757-9 PMID: 1465147
  29. Accumulation of passively transferred primed T cells independently of their antigen specificity following central nervous system trauma.
    J Neuroimmunol. 1998 Aug 14;89(1-2):88-96 PMID: 9726830
  30. Brain-derived neurotrophic factor rescues spinal motor neurons from axotomy-induced cell death.
    Nature. 1992 Dec 24-31;360(6406):753-5 PMID: 1281520
  31. Potential treatment modalities for glaucomatous neuropathy: neuroprotection and neuroregeneration.
    J Glaucoma. 1996 Dec;5(6):427-32 PMID: 8946301
  32. Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy.
    Nat Med. 1999 Jan;5(1):49-55 PMID: 9883839
  33. Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1.
    J Neuroimmunol. 1998 Nov 2;91(1-2):135-46 PMID: 9846830
Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
2000-06-20
Pages
7446-51
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC16565
Subset
IM
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