Monocyte chemoattractant protein-1 enhances HSV-induced encephalomyelitis by stimulating Th2 responses

Hideto Nakajima, Makiko Kobayashi, Richard B. Pollard, Fujio Suzuki

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

Monocyte chemoattractant protein (MCP)-1 has a pathogenic role in herpesvirus-induced encephalomyelitis (HSM). Anti-MCP-1 antibody greatly decreased HSM severity in mice infected with herpes simplex virus type 2 (HSM mice), compared with its effect in control HSM mice treated with rabbit immunoglobulin. HSM severity was markedly enhanced in mice previously treated with a mixture of interleukin (IL) 4 and -10. In response to stimulation with antigen, HSM mouse cells isolated from cerebrospinal fluids (CSF cells) produced IL-4 in culture fluids; however, IL-4 production decreased in CSF cells derived from HSM mice previously treated with anti-MCP-1 antibody. A macrophage population isolated in CSF cells from HSM mice (CSF-Mφ) produced MCP-1 in culture fluids. In response to stimulation with herpesvirus antigen, a population of T cells isolated from CSF cells from HSM mice (CSF-T cells) produced IL-4 into their culture fluids, although MCP-1 was not produced by CSF-T cells stimulated by this antigen. IL-4 production by CSF-T cells was markedly enhanced when they were stimulated with viral antigen in the presence of murine recombinant MCP-1 (rMCP-1). Furthermore, IL-4 was produced in naive splenic T cells cocultured with CSF-Mφ. These results indicate that the severity of HSM is influenced by MCP-1, which stimulates Th2 responses.

Original languageEnglish (US)
Pages (from-to)374-380
Number of pages7
JournalJournal of Leukocyte Biology
Volume70
Issue number3
StatePublished - 2001
Externally publishedYes

Keywords

  • Cerebrospinal fluids
  • Herpes simplex virus type 2
  • Interleukin 4
  • MCP-1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

Fingerprint

Dive into the research topics of 'Monocyte chemoattractant protein-1 enhances HSV-induced encephalomyelitis by stimulating Th2 responses'. Together they form a unique fingerprint.

Cite this