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and Nitric Oxide Synthetase 21
*
Institute for Experimental Immunology, Zürich, Switzerland;
Basel Institute for Immunology, Basel, Switzerland;
Department of Pathology, University of Freiburg, Freiburg, Germany; and
§
Max Planck Institute for Immunobiology, Freiburg, Germany
Resistance or susceptibility to most infectious diseases is
strongly determined by the balance of type 1 vs type 2 cytokines
produced during infection. However, for viruses, this scheme may be
applicable only to infections with some cytopathic viruses, where
IFN-
is considered as mandatory for host defense with little if any
participation of type 2 responses. We studied the role of signature Th1
(IL-12, IFN-) and Th2 (IL-4, IL-10) cytokines for immune responses
against vaccinia virus (VV). IL-12-/- mice were far more
susceptible than IFN--/- mice, and primary CTL
responses against VV were absent in IL-12-/- mice but
remained intact in IFN--/- mice. Both CD4+
and CD8+ T cells from IL-12-/- mice were
unimpaired in IFN- production, although CD4+ T cells
showed elevated Th2 cytokine responses. Virus replication was impaired
in IL-4-/- mice and, even more strikingly, in
IL-10-/- mice, which both produced elevated levels of the
proinflammatory cytokines IL-1
and IL-6. Thus, IL-4 produced by Th2
cells and IL-10 produced by Th2 cells and probably also by macrophages
counteract efficient anti-viral host defense. Surprisingly, NO
production, which is considered as a major type 1 effector pathway
inhibited by type 2 cytokines, appears to play a limited role against
VV, because NO sythetase 2-deficient mice did not show increased viral
replication. Thus, our results identify a new role for IL-12 in defense
beyond the induction of IFN- and show that IL-4 and IL-10 modulate
host protective responses to VV.
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