Candida albicans has evolved immune evasion strategies that include cell wall remodelling via masking or shaving of pathogen-associated molecular pattern (PAMP) β-1,3-glucan. Previously we showed that C. albicans exploits a range of host-derived signals to induce the production of glucanases to clip off superficial β-1,3-glucan strands at the cell surface in an attempt to evade phagocytic uptake [Nature Micro 2, 16238; mBio 9, e01318-18; Nature Comms 10, 5315]. Here, we show that adaptation to niche-simulating conditions modulates the exposure of mannan-related PAMPs at the C. albicans cell surface. Mannans are complex, comprising linear and branched polymers of mannose. Mannans are recognised by a range of C-lectin type receptors, including CRD4-7 (mannose receptor), DC-SIGN and dectin-2. However, the chemical nature of their mannan ligands and their location in the fungal cell wall are not accurately defined. In this study, we examined the impact of growing C. albicans in plasma-, vagina-, saliva- and gut-simulating media upon PAMP exposure and immune recognition. Standard laboratory media (SD and YPD) were used as controls. Using a combination of flow cytometry, fluorescent microscopy, TEM, cytokine assays, and neutrophil killing assays, we have shown that C. albicans cells exhibit significant differences in the exposure of mannan ligands on the cell surface depending on the growth conditions. These changes in PAMP exposure correlated with differential cytokine responses, as well as altered sensitivities to stresses and antifungals. Our data reinforce the view that adaptation to niche-simulating conditions makes C. albicans a moving target for the immune system.