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*
Department of Microbiology, Montana State University, Bozeman, MT 59717;
Department of Microbiology, School of Medicine, and Cell and Molecular Biology Program, University of Nevada, Reno, NV 89557; and
Department of Pathology, Harvard Medical School, Boston, MA 02115
The incidence of life-threatening, hematogenously disseminated
candidiasis, which is predominantly caused by Candida
albicans, parallels the use of modern medical procedures that
adversely affect the immune system. Limited antifungal drug choices and
emergence of drug-resistant C. albicans strains indicate
the need for novel prevention and therapeutic strategies. We are
developing vaccines and Abs that enhance resistance against
experimental candidiasis. However, the prevalence of serum
anti-Candida Abs in candidiasis patients has led to
the misconception that Abs are not protective. To explain the apparent
discrepancy between such clinical observations and our work, we
compared functional activities of C. albicans-specific
protective and nonprotective mAbs. Both kinds of Abs are agglutinins
that fix complement and are specific for cell surface mannan, but the
protective Abs recognize 
-mannan, and the nonprotective Ab is
specific for 
-mannan. By several indirect and direct measures, the
protective mAbs more efficiently bind complement factor C3 to the yeast
cell than do nonprotective Ab. We hypothesize that the C3 deposition
causes preferential association of blood-borne fungi with host
phagocytic cells that are capable of killing the fungus. We conclude
from these results that the protective potential of Abs is dependent on
epitope specificity, serum titer, and ability to rapidly and
efficiently fix complement to the fungal surface. The mechanism of
protection appears to be associated with enhanced phagocytosis and
killing of the fungus.
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