T cell independent mechanism for copolymer-1-induced neuroprotection

Jianuo Liu, Thomas V. Johnson, Jamie Lin, Servio H. Ramirez, Tatiana K. Bronich, Steve Caplan, Yuri Persidsky, Howard E. Gendelman, Jonathan Kipnis

Research output: Contribution to journalArticlepeer-review

62 Scopus citations


Despite active investigation of copolymer-1 (Cop-1) for nearly 40 years the mechanisms underlying its neuroprotective properties remain contentious. Nonetheless, current dogma for Cop-1 neuroprotective activities in autoimmune and neurodegenerative diseases include bystander suppression of autoimmune T cells and attenuation of microglial responses. In this report, we demonstrate that Cop-1 interacts directly with primary human neurons and decreases neuronal cell death induced by staurosporine or oxidative stress. This neuroprotection is mediated through protein kinase Ca and brain- derived neurotrophic factor. Dendritic cells (DQ uptake Cop-1, deliver it to the injury site, and release it in an active form. Interactions between Cop-1 and DC enhance DC blood brain barrier migration. In a rat model with optic nerve crush injury, Cop-1- primed DC induce T cell independent neuroprotection. These findings may facilitate the development of neuroprotective approaches using DC-mediated Cop-1 delivery to diseased nervous tissue.

Original languageEnglish (US)
Pages (from-to)3143-3154
Number of pages12
JournalEuropean Journal of Immunology
Issue number11
StatePublished - Nov 2007


  • Dendritic cells
  • Inflammation
  • Neuroimmunology
  • T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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