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Candida albicans is a comensal microorganism that under certain circumstances is able to transform into a pathogen. This ability to switch constitute a virulence factor that C. albicans uses to invade and spread. The innate immune system recognize the different forms of C. albicans activating receptors (PRRs) that recognize PAMPs or conserved molecular patterns. The most impor tant immune cells are macrophages and neutrophils that generate an effector response through phagocytosis and oxidative burst against C. albicans. Dendritic cells express the most of PRRs involved in the recognition of C. albicans activating the cytokines synthesis forward to a TH1 (induced by INF tipo1, IL-12, INFγ), Treg (induced by TGFβ, IL-10) y TH17 (induced by IL- 23, IL6) immune response. Epithelial cells not only constitute a physical barrier against C. albicans, but they are crucial in the first recognition of this microorganism. Through a biphasic response these cells differentially activate pathways that determine a no cytokine response when blastoconidia (commensal form) is present and an inflammatory response in presence of hyphae (pathogenic form). C. albicans develops immune evasive mechanism. This complex host-fungi interaction determines if the host will eradicate the infection or if this microorganism will invade the host, expressing it virulence. [ABSTRACT FROM AUTHOR]