An association between morphogenesis and virulence has long been presumed for dimorphic fungi that are pathogenic to humans, as one morphotype exists in the environment or during commensalism, and another within the host during the disease process. For Candida albicans, putative virulence factors include the ability to switch between saprophytic yeast and pathogenic, filamentous forms of the fungus. Dendritic cells sense either form in a specific way, resulting in distinct, T-helper-cell-dependent protective and non-protective immunities. Recent evidence suggests that the use of distinct recognition receptors contributes to the disparate patterns of reactivity observed locally in response to challenge with C. albicans. These findings offer new interpretive clues to the mechanisms of fungal virulence: rather than dimorphism per se, the engagement of different recognition receptors on dendritic cells might select the mode of fungal internalization and antigen presentation, condition the nature of the T-helper response and, ultimately, favor saprophytism or infection.