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CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelination.

Abstract：

:Demyelination, a pathological hallmark of multiple sclerosis, may be a necessary but not a sufficient condition for motor dysfunction associated with this disease. We favor a neurodegenerative model of multiple sclerosis and suggest that demyelination creates a permissive environment wherein the denuded axon becomes susceptible to immune-mediated injury. Unfortunately, the cellular effectors responsible for eliciting such axonal injury are currently unknown. Based on previous observations implicating cytotoxic T cells in this injury, we assessed motor function, axon dropout, and axon injury following peptide depletion of the immunodominant CD8+ antiviral T cell response in the IFNgamma receptor-deficient mouse model of acute demyelination. We found that the targeted removal of this population of cytotoxic effector cells prior to infection with the Theiler's murine encephalomyelitis virus caused a substantial preservation of motor function at 45 days postinfection that was associated with preservation of retrograde axonal transport in a subpopulation of surviving axons within the spinal cord. We conclude that cytotoxic T cells may be responsible for the initiation of axon injury following demyelination.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Howe CL,Ure D,Adelson JD,LaFrance-Corey R,Johnson A,Rodriguez M

doi

10.1016/j.jneuroim.2007.04.005

subject

Has Abstract

pub_date

2007-08-01 00:00:00

pages

13-21

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(07)00124-5

journal_volume

188

pub_type

杂志文章

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