CCR2 regulates development of Theiler's murine encephalomyelitis virus-induced demyelinating disease

Jami L. Bennett, Adam Elhofy, Israel Charo, Stephen D. Miller, Mauro C. Dal Canto, William J. Karpus*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Theiler's murine encephalomyelitis virus (TMEV)-iriduced demyelinating disease, a murine model for multiple sclerosis, involves recruitment of T cells and macrophages to the CNS after infection. We hypothesized that CCR2, the only known receptor for CCL2, would be required for TMEV-induced demyelinating disease development because of its role in macrophage recruitment. TMEV-infected SJL CCR2 knockout (KO) mice showed decreased long-term clinical disease severity and less demyelination compared with controls. Flow cytometric data indicated that macrophages (CD45highCD11b+) in the CNS of TMEV-infected CCR2 KO mice were decreased compared with control mice throughout disease. CD4+ and CD8+ T cell percentages in the CNS of TMEV-infected control and CCR2 KO mice were similar over the course of disease. There were no apparent differences between CCR2 KO and control peripheral immune responses. The frequency of interferon-γ-producing T cells in response to proteolipid protein 139-151 in the CNS was also similar during the autoimmunity stage of TMEV-induced demyelinating disease. These data suggest that CCR2 is important for development of clinical disease by regulating macrophage accumulation after TMEV Infection.

Original languageEnglish (US)
Pages (from-to)19-33
Number of pages15
JournalViral Immunology
Issue number1
StatePublished - 2007

ASJC Scopus subject areas

  • Immunology
  • Molecular Medicine
  • Virology

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