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,*
Departments of
*
Immunology and
Molecular Biology, Division of Virology, The Scripps Research Institute, La Jolla, CA 92037
Herpesviruses utilize many strategies for weakening the host immune
response. For CMV, this includes avoidance of NK clearance and
inhibition of MHC class I and class II presentation pathways. In this
study, we report that mouse CMV (MCMV) specifically causes a premature
and transient activation of host IL-10 very early in the course of
infection, resulting in a dramatic and selective reduction in MHC class
II surface expression. The expression of IL-10 is normally late in the
immune response to a pathogen, serving to dampen the response by
suppression of the production of inflammatory cytokines. In infection
of macrophages, we show that MCMV induces the production of IL-10,
leading to an early and selective reduction in the expression of MHC
class II on the surface of the cells. Inhibition of MHC class II
expression was not observed in the presence of neutralizing Abs to
IL-10 or in macrophages from IL-10-deficient mice. Moreover,
MCMV-infected IL-10-deficient mice developed an early and significantly
more robust macrophage MHC class II induction than normal mice.
Altogether, our results demonstrate that viral induction of an IL-10
autocrine pathway plays an essential early role in selectively reducing
MHC class II expression on the surface of APC prior to stimulation by
IFN-
.
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