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Cutting Edge |
Departments of
*
Pathology and
Molecular Microbiology and Immunology, Johns Hopkins Medical Institutions, Baltimore, MD 21205
Appropriate treatment of autoimmune myocarditis following virus
infection remains a major clinical problem. Induction of nasal
tolerance may provide a new approach to treatment. However, the exact
mechanism of nasal tolerance is unknown. To assess the mechanism of
nasal tolerance, we examined the role of IL-10 in the induction and
suppression of autoimmune myocarditis. First we showed that blocking
IL-10 concurrent with nasal administration of Ag abolished the
disease-suppressing effect of nasal tolerization. It also led to
increased cardiac myosin-specific IL-1 and TNF-
production. Then we
demonstrated that blocking IL-10 during the effector phase increased
not only the incidence and severity of disease but also Ag-specific
IL-2, IL-4, and TNF- production as well as cardiac myosin-specific
IgG1 and IgG2b production, whereas blocking IL-10 during the induction
phase had no effect. This study implicates IL-10 in the induction of
nasal tolerance and in limiting inflammation later during the disease
process.
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