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Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205
SJL mice are susceptible to inflammatory autoimmune diseases of the
central nervous system (CNS), while BALB/c mice are relatively
resistant. To understand differences in immune responses that may
contribute to autoimmune neurologic disease, we compared the responses
of SJL and BALB/c mice to infection with Sindbis virus, a virus that
causes acute nonfatal encephalomyelitis in both strains of mice.
Clearance of virus was similar, but SJL mice developed a more intense
inflammatory response in the brain and spinal cord and inflammation
persisted for several weeks. Analysis of lymphocytes isolated from
brains early after infection showed an absence of NK cells in SJL mice,
while both strains of mice showed CD4+ and CD8+
T cells. During the second week after infection, CD4+ T
cells increased in SJL mice and the proportion of CD8+ T
cells decreased, while the opposite pattern was seen in BALB/c mice.
Expression of IL-10 mRNA was higher and IL-4 mRNA was lower in the
brains of infected SJL than in BALB/c mice, while expression of the
mRNAs of IL-6, IL-1ß, TNF
, and the Th1 cytokines IL-2, IL-12, and
IFN-
was similar. Lymphocytes isolated from the CNS of SJL mice
produced large amounts of IL-10. CNS lymphocytes from both strains of
mice produced IFN- in response to stimulation with Sindbis virus,
but not in response to myelin basic protein. These data suggest that
IL-10-producing CD4+ T cells are differentially recruited
to or regulated within the CNS of SJL mice compared with BALB/c mice
infected with Sindbis virus, a characteristic that may be related to
low levels of IL-4, and is likely to be involved in susceptibility of
SJL mice to CNS inflammatory diseases.
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