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*
Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy;
The Wistar Institute, Philadelphia, PA 19104; and
Roche Milano Ricerche, Milan, Italy
IL-12 is both required and prognostic for Th1 development in mice
with Candida albicans infection. To delineate further
the physiologic role of IL-12 in antifungal immunity, mice deficient
for this cytokine were assessed for susceptibility to C.
albicans infections, and for parameters of innate and adaptive
immunity. IL-12-deficient mice were highly susceptible to
gastrointestinal infection or to reinfection and showed elevated
production of Candida-specific IgE and IL-4 and
defective production of IFN-
. The failure to mount protective Th1
responses occurred despite the presence of an unimpaired innate
antifungal immune response, which correlated with unaltered IFN-
production, but defective production of, and responsiveness to,
inhibitory IL-10. IL-10 or IL-12 neutralization increased the innate
antifungal resistance in wild-type mice. However, in IL-12-deficient
mice, treatment with exogenous IL-12 or IL-10 impaired IL-4 production
and increased resistance to infection, through a negative effect on the
CTLA-4/B7-2 costimulatory pathway. These results confirm the obligatory
role of IL-12 in the induction of anticandidal Th1 responses, and
indicate the existence of a positive regulatory loop between IL-12 and
IL-10 that may adversely affect the innate antifungal response, but is
required for optimal costimulation of IL-12-dependent
CD4+Th1 cells.
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