CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease

Chad Laurie, Ashley Reynolds, Ozlem Coskun, Erik Bowman, Howard Eliot Gendelman, R Lee Mosley

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

Adoptive transfer of lymphoid cells from Copolymer 1 (Cop-1) immunized mice leads to T cell accumulation within the substantia nigra, modulation of microglial responses, upregulation of glial cell derived neurotrophic factor, and protection of the nigrostriatum following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication. We now demonstrate that T cells isolated from lymph nodes and spleens of Cop-1 immunized animals protect the nigrostriatal system from MPTP-induced neurodegeneration in a dose-dependent manner. CD4+ T cells elicited the most significant neuroprotective response while high titers of anti-Cop-1 antibodies showed no effect. These data further support the use of immunomodulatory strategies for Parkinson's disease.

Original languageEnglish (US)
Pages (from-to)60-68
Number of pages9
JournalJournal of Neuroimmunology
Volume183
Issue number1-2
DOIs
StatePublished - Feb 1 2007

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Dopaminergic Neurons
Parkinson Disease
T-Lymphocytes
Adoptive Transfer
Nerve Growth Factors
Substantia Nigra
Neuroglia
Up-Regulation
Spleen
Lymph Nodes
Lymphocytes
Antibodies

Keywords

  • CD4 T cells
  • Copolymer-1
  • Immunomodulation
  • MPTP
  • Neuroprotection
  • Parkinson's disease

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

CD4+ T cells from Copolymer-1 immunized mice protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease. / Laurie, Chad; Reynolds, Ashley; Coskun, Ozlem; Bowman, Erik; Gendelman, Howard Eliot; Mosley, R Lee.

In: Journal of Neuroimmunology, Vol. 183, No. 1-2, 01.02.2007, p. 60-68.

Research output: Contribution to journalArticle

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