The molecular interactions between commensal microorganisms and their host are basically different from those triggered by pathogens since they involve tolerance. When the commensal is genetically equipped to become an opportunistic pathogen, as is the case with Candida albicans, the picture becomes more complex. In this case, the balance between protection and invasion depends on host reactivity to altered microbial expression of ligands interacting with innate immune sensors. Based on experimental evidence obtained with C. albicans, we discuss the different molecular processes involved in the sensing of this important opportunistic human pathogen by a panel of pattern recognition receptors (PRRs) according to the numerous pathogen-associated molecular patterns (PAMPs) that can be exposed at its surface. Beneficial or deleterious immune responses that either maintain a commensal state or favour damage by the yeast result from this dynamic interplay.