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

被引:238
作者
Kipnis, J
Yoles, E
Porat, Z
Cohen, A
Mor, F
Sela, M
Cohen, IR
Schwartz, M [1 ]
机构
[1] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel
[2] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel
[3] Proneuron Ltd, Ness Ziona, Israel
关键词
D O I
10.1073/pnas.97.13.7446
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 he 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.
引用
收藏
页码:7446 / 7451
页数:6
相关论文
共 34 条
[1]   T-SUPPRESSOR HYBRIDOMAS AND INTERLEUKIN-2-DEPENDENT LINES INDUCED BY COPOLYMER-1 OR BY SPINAL-CORD HOMOGENATE DOWN-REGULATE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS [J].
AHARONI, R ;
TEITELBAUM, D ;
ARNON, R .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (01) :17-25
[2]   Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1 [J].
Aharoni, R ;
Teitelbaum, D ;
Sela, M ;
Arnon, R .
JOURNAL OF NEUROIMMUNOLOGY, 1998, 91 (1-2) :135-146
[3]   Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis [J].
Aharoni, R ;
Teitelbaum, D ;
Sela, M ;
Arnon, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (20) :10821-10826
[4]  
BENNUN A, 1982, J IMMUNOL, V129, P303
[5]   The autoimmune reactivity to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis is potentially pathogenic: Effect of copolymer 1 on MOG-induced disease [J].
BenNun, A ;
Mendel, I ;
Bakimer, R ;
FridkisHareli, M ;
Teitelbaum, D ;
Arnon, R ;
Sela, M ;
deRosbo, NK .
JOURNAL OF NEUROLOGY, 1996, 243 (04) :S14-S22
[6]   THE RAPID ISOLATION OF CLONABLE ANTIGEN-SPECIFIC LYMPHOCYTE-T LINES CAPABLE OF MEDIATING AUTOIMMUNE ENCEPHALOMYELITIS [J].
BENNUN, A ;
WEKERLE, H ;
COHEN, IR .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1981, 11 (03) :195-199
[7]  
DUVDEVANI R, 1990, RESTOR NEUROL NEUROS, V2, P31, DOI 10.3233/RNN-1990-2104
[8]   Binding of random copolymers of three amino acids to class II MHC molecules [J].
Fridkis-Hareli, M ;
Aharoni, R ;
Teitelbaum, D ;
Arnon, R ;
Sela, M ;
Strominger, JL .
INTERNATIONAL IMMUNOLOGY, 1999, 11 (05) :635-641
[9]  
GILLIS S, 1978, J IMMUNOL, V120, P2027
[10]   Autoimmune T cells as potential neuroprotective therapy for spinal cord injury [J].
Hauben, E ;
Nevo, U ;
Yoles, E ;
Moalem, G ;
Arganov, E ;
Mor, F ;
Akselrod, S ;
Neeman, M ;
Cohen, IR ;
Schwartz, M .
LANCET, 2000, 355 (9200) :286-287