Mucosal tissues are constitutively colonized by a wide assortment of host-adapted microbes. This includes the polymorphic fungus Candida albicans which is a primary target of human adaptive responses. Immunogenicity is replicated after intestinal colonization in preclinical models with a surprising array of protective benefits for most hosts, but harmful consequences for a few. The interaction between fungus and host is complex, and traditionally, the masking of antigenic fungal ligands has been viewed as a tactic for fungal immune evasion during invasive infection. However, we propose that dynamic expression of cell wall moieties, host cell lysins, and other antigenic C. albicans determinants is necessary during the more ubiquitous context of intestinal colonization to prime immunogenicity and optimize mammalian host symbiosis.