Disseminated candidiasis occurs in 11-27% of patients with protracted neutropenia from acute leukemia or bone marrow transplantation [12], resulting in mortality which may approach 95% [104]. Candidemia with haematogenously disseminated candidiasis and other serious Candida infections are also encountered increasingly in seriously ill hospitalized patients without classic immunocompromising diseases [32, 165,166], thus extending the significance of the problem from occurrence exclusively in patients with relatively unusual and rapidly fatal diseases. Organisms of the genus Candida are now the third most commonly isolated from blood cultures [73], resulting in an attributable mortality of 38% in non-neutropenic hosts [166]. In specific patient populations, symptomatic oral or esophageal infections may develop from gastrointestinal (GI) proliferation of Candida [13, 110]. Candida colonization and infection of the GI tract are also important as the portal of entry for most episodes of disseminated candidiasis in neutropenic patients [13], as highlighted by hepatosplenic candidiasis [154]. Because of this increasing clinical importance of Candida infections, it is imperative to pursue understanding of the interaction between this parasite and host defense systems. The purpose of this review is to present an overview of these interactions, highlighting what has been learned from in vitro experiments, from animal model studies, and from careful analyses of human candidiasis. This review does not purport to be allinclusive; relevant reviews of specific areas of Candida-host defense system interactions which pursue specific topics in further depth are cited throughout. Rather, this author's interpretation of the sufficiencies and deficiencies of available data are used to develop a model of these interactions for further analyses. Candida species colonize mucocutaneous surfaces and most infections arise endogenously from this source [32, 122]. This was initially determined by the observation of colonization preceding invasive infection [39] and has been confirmed recently by molecular epidemiology based on DNA typing [152[. It is therefore imperative to first review defense system interactions in mucocutaneous candidiasis. Candida species do not normally grow on skin [32]. It has been presumed that lipid components such as free fatty acids are primarily responsible for this inhibitory activity on normal skin. However, recently a >300 kDa protein and a 49 kDa protein were isolated from terminally differentiated corneocytes of rat skin and were demonstrated to