Immune evasion of the human pathogenic yeast Candida albicans

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Candida albicans is the most common human pathogenic yeast and causes cutanous and mucocutanous candidiasis. This dimorphic yeast causes life threatening systemic infections especially in immunocompromised and granulocytopenic patients. During infection candida is exposed to the human immune systems and is attacked by the complement system, which represents the early acting part of innate immunity. It is currently unclear how candida controls and evades complement activation. Initially the presence of host like complement receptors CR2 and CR3 (CD11b/CD18) were reported on the surface of the yeast, however none of these molecules has been identified in molecular terms so far. Recently, attachment of host immune regulators and complement inhibitors Factor H, FHL-1 and C4BP to the surface of candida have been shown to mediate complement and immune evasion. In the proposed project we want to characterize the role of the attached immune regulators in molecular terms and define the cellular and immunological consequences for survival and immune escape of candida. Cloning of the molecules which mediate attachment of host regulators on the candida surface and analyzing the role of the selectively attached host immune regulators for host yeast interaction will describe a novel immune evasion mechanism of candida. This approach is expected to identify new virulence factor(s) and thus define novel targets of the pathogenic yeast for drug development.