Candida albicans (C. albicans) is a microorganism belonging to the commensal flora of the intestinal, oral and vaginal mucosal surfaces in healthy humans. This commensalism results from a balance between the virulence factors of the yeast and defense mechanisms of the host. However, disturbance of this balance in a vulnerable patient may result in intense mucosal colonization that promotes invasion of epithelial cells, translocation across the intestinal epithelial barrier and, eventually hematogenous dissemination. A better understanding of the mechanisms by which C. albicans interacts with the intestinal mucosa will improve our knowledge of the physiopathology of disseminated candidiasis. Mucosal immunity contributes to both commensalism and pathogenicity of the fungus, possibly through presentation of C. albicans antigens to the underlying organized lymphoid structures via transcytosis, mediated by the specialized epithelial M cells. With this aim, we developed an in vitro model of the human intestinal Follicle Associated Epithelium (FAE) where enterocytes of the Caco-2 cell line in close contact with mucosal lymphocytes differentiate in M cells. Studying adherence, invasion and translocation of C. albicans across co-cultures suggests that C. albicans interacts differentially with M cells / enterocytes co-cultures compared to monolayers of Caco-2 cells alone. The uptake mechanism allowing C. albicans to translocate across the co- culture model is under investigation, as well as the respective contribution of the yeast and hyphal forms to this process using KO mutants of C. albicans unable to produce hyphae. Finally the cytokine production by intestinal cells resulting from C. albicans and M cells / Caco-2 co-cultures interaction will be studied.