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J Neurovirol. 2006 Aug;12(4):251-61.

Anti-CCL2 treatment inhibits Theiler's murine encephalomyelitis virus-induced demyelinating disease.

Author information

1
Department of Pathology, Immunobiology Center, Robert H. Lurie Cancer Center, Institute for Neuroscience, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611, USA. w-karpus@northwestern.edu

Abstract

Theiler's murine encephalomyelitis virus induces a demyelinating disease (TMEV-IDD) of the central nervous system (CNS) in susceptible mouse strains with accompanying histopathology characterized by mononuclear cell infiltrates. In susceptible strains of mice such as SJL, virus establishes a persistent infection in macrophages, induces a CNS infiltration by macrophages, T cells, and B cells, which results in chronic-progressive paralysis. In the present report the authors have investigated the functional role of CCL2 (monocyte chemotactic protein-1) in the induction and progression of demyelinating disease. Treatment of infected mice at day 0, 14, or 28 with anti-CCL2 resulted in a significant decrease in the clinical disease progression. Further analysis of anti-CCL2-treated mice revealed decreased CNS inflammation and mononuclear cell infiltration with an accompanying change in inflammatory cytokine responses. There was an overall decrease in the absolute numbers of CNS-infiltrating CD4+ T cells, macrophages, and B cells. Finally, anti-CCL2 treatment resulted in decreased viral load in the CNS. These data directly demonstrate a role for CCL2 in the pathogenesis of TMEV-IDD.

PMID:
16966216
PMCID:
PMC4040265
DOI:
10.1080/13550280600873819
[Indexed for MEDLINE]
Free PMC Article

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