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* Microbiology Section, Department of Experimental Medicine and Biochemical Science, University of Perugia, Perugia, Italy;
Microbiology Section, Department of Experimental Medicine, University of Rome, Rome, Italy; and
Immunology Research Division, Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115
Protective immunity to the fungus Candida albicans
is mediated by Ag-specific Th1 cells. Paradoxically, some Th2 cytokines
are required for the maintenance of Th1-mediated immune resistance to
the fungus. Therefore, in addition to the Th1/Th2 balance, other
mechanisms seem to be involved in the regulation of Th1 immunity to the
fungus. Here we show that CD4+CD25+ T cells,
negatively regulating antifungal Th1 reactivity, are generated in mice
with candidiasis. CD4+CD25+ T cells were not
generated in B7-2- or CD28-deficient mice or in condition of IL-10
signaling deficiency. Accordingly, although capable of efficiently
restricting the fungal growth, these mice experienced inflammatory
pathology and were incapable of resistance to reinfection.
CD4+CD25+ T cells poorly proliferated in vitro;
were highly enriched for cells producing IL-4, IL-10, and TGF-
; and
required IL-10-producing, Candida hypha-activated
dendritic cells for generation. Adoptive transfer of
CD4+CD25+ T cells or IL-10-producing dendritic
cells restored resistance to reinfection and decreased inflammation in
B7-2-deficient mice. These results show that oral tolerance
induced by Candida hyphae is required for the occurrence
of long-lasting protective immunity after yeast priming. The
implication is that preventing reactivation rather than favoring
sterilizing immunity to ubiquitous fungal pathogens may represent the
ultimate expectation of vaccine-based
strategies.
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