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Is Required for IL-12 Responsiveness in Mice with Candida albicans Infection1
*
Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy; and
Basel Institute of Immunology, Basel, Switzerland
To elucidate the role of IFN-
in antifungal CD4+
Th-dependent immunity, 129/Sv/Ev mice deficient for IFN- receptor
(IFN-R-/-) were assessed for susceptibility to
gastrointestinal or systemic Candida albicans infection
and for parameters of innate and adaptive T helper immunity.
IFN-R-/- mice failed to mount protective Th1-mediated
acquired immunity upon mucosal immunization or in response to a live
vaccine strain of the yeast. The impaired Th1-mediated resistance
correlated with defective IL-12 responsiveness, but not IL-12
production, and occurred in the presence of an increased innate
antifungal resistance. The development of nonprotective Th2 responses
was observed in IFN-R-/- mice upon mucosal infection
and subsequent reinfection. However, under experimental conditions of
Th2 cell activation, the occurrence of Th2 cell responses was similar
in IFN-R-/- and in IFN-R+/+ mice. These
results indicate the complex immunoregulatory role of IFN- in the
induction of mucosal and nonmucosal anticandidal Th cell responses;
IFN- is not essential for the occurrence of Th2 responses but is
required for development of IL-12-dependent protective Th1-dependent
immunity.
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