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Monocyte chemoattractant protein‐1 enhances HSV‐induced encephalomyelitis by stimulating Th2 responses
Author(s) -
Nakajima Hideto,
Kobayashi Makiko,
Pollard Richard B.,
Suzuki Fujio
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.3.374
Subject(s) - biology , chemotaxis , monocyte , immunology , encephalomyelitis , virology , microbiology and biotechnology , genetics , receptor , multiple sclerosis
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.