T cell immunity to copolymer 1 confers neuroprotection on the damaged optic nerve: possible therapy for optic neuropathies.
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.
Kipnis
J
J
Departments of Neurobiology and Immunology, The Weizmann Institute of Science, 76100 Rehovot, Israel.
Yoles
E
E
Porat
Z
Z
Cohen
A
A
Mor
F
F
Sela
M
M
Cohen
I R
IR
Schwartz
M
M
D000818:Animals; D017951:Antigen Presentation; D005260:Female; D000068717:Glatiramer Acetate; D007111:Immunity, Cellular; D016219:Immunotherapy, Adoptive; D009900:Optic Nerve / Q000276:immunology* / Q000473:pathology; D009901:Optic Nerve Diseases / Q000276:immunology* / Q000628:therapy*; D010455:Peptides / Q000008:administration & dosage* / Q000276:immunology*; D051381:Rats; D011917:Rats, Inbred Lew; D013601:T-Lymphocytes / Q000276:immunology*
D010455:Peptides; D000068717:Glatiramer Acetate