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Department of Microbiology and Immunology, Loyola University Chicago Medical Center, Maywood, IL 60153
Infection with pathogens often leads to loss of body weight, but
the cause of weight loss during infection is poorly understood. We used
the infection of mice with lymphocytic choriomeningitis virus (LCMV) as
a model to study how pathogens induce weight loss. If LCMV is
introduced into the CNS of CTL-deficient mice, the immune response
against the virus leads to a severe weight loss called wasting disease.
We planned to determine what components of this antiviral immune
response mediate wasting disease. By adoptive transfer, we show that
CD4 T cells activated by LCMV infection are sufficient to cause wasting
disease. We examined the role of cytokines in LCMV-induced wasting
disease using mice lacking specific cytokines or cytokine receptors.
Results of adoptive transfer experiments suggest that TNF-
is not
involved in LCMV-induced wasting disease and show that IFN-
contributes to the disease. Consistent with a role for IFN- in
wasting, we find that IFN- is necessary for LCMV-specific CD4 T cell
responses in the CNS, most likely because it is required to induce MHC
class II expression. Our data also indicate that IL-1 is required for
LCMV-induced wasting and that IL-6 contributes to the wasting disease.
Additionally, our results identify -melanocyte-stimulating hormone
as a potential mediator of the disease. Overall, this work defines the
critical role of virus-primed CD4 T cells and of proinflammatory
cytokines in the pathogenesis of wasting disease induced by LCMV
infection.
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