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* Department of Experimental Medicine and Biochemical Science, University of Perugia, Perugia, Italy;
Department of Environmental Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland; and
Immunology Research Division, Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115
To find out whether polymorphonuclear neutrophils (PMN), abundantly
recruited in disseminated Candida albicans infection,
could directly affect the activation of Th cells we addressed the
issues as to whether murine PMN, like their human counterparts, express
costimulatory molecules and the functional consequence of this
expression in terms of antifungal immune resistance. To this purpose,
we assessed 1) the expression of CD80 (B7-1) and CD86 (B7-2) molecules
on peripheral, splenic, and inflammatory murine Gr-1+ PMN;
2) its modulation upon interaction with C. albicans in
vitro, in vivo, and in human PMN; 3) the effect of
Candida exposure on the ability of murine PMN to affect
CD4+ Th1 cell proliferation and cytokine production; and 4)
the mechanism responsible for this effect. Murine PMN constitutively
expressed CD80 molecules on both the surface and intracellularly;
however, in both murine and human PMN, CD80 expression was
differentially modulated upon interaction with Candida
yeasts or hyphae in vitro as well as in infected mice. The expression
of the CD86 molecule was neither constitutive nor inducible upon
exposure to the fungus. In vitro, Gr-1+ PMN were found to
inhibit the activation of IFN-
-producing CD4+ T cells
and to induce apoptosis through a CD80/CD28-dependent mechanism. A
population of CD80+Gr-1+ myeloid cells was
found to be expanded in conventional as well as in bone
marrow-transplanted mice with disseminated candidiasis, but its
depletion increased the IFN--mediated antifungal resistance. These
data indicate that alternatively activated PMN expressing CD80 may
adversely affect Th1-dependent resistance in fungal
infections.
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