Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical Branch, Galveston
Correspondence: Dr. Fujio Suzuki, Department of Internal Medicine, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0435. E-mail: fsuzuki{at}utmb.edu
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-M
) 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-M
. These results indicate that the severity of HSM is influenced
by MCP-1, which stimulates Th2 responses.
Key Words: cerebrospinal fluids herpes simplex virus type 2 interleukin 4 MCP-1
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