Micafungin belongs to the antifungal family of echinocandins, which act as non-competitive inhibitors of the fungal cell-wall β-1,3-D-glucan synthase. Since C. albicans is the most prevalent pathogenic fungus in humans, we study the involvement of Micafungin in the modulation of the inflammatory response developed by human tissue macrophages against C. albicans. The MIC for Micafungin was 0.016 μg/ml on the C. albicans SC5314 standard strain. Micafungin induced a drastic reduction in the number of exponential SC5314 viable cells, the fungicidal effect being dependent on the cellular metabolic activity. Notably, Micafungin also caused a structural remodelling of the cell wall, leading to exposure of the β-glucan and chitin content on the external surface. At the higher doses used (0.05 μg/ml), the antifungal also induced the blowing up of budding yeasts. In addition, preincubation with Micafungin before exposure to human tissue macrophages enhanced the secretion of TNF-α, IL-17A and IL-10 cytokines. Our results strongly suggest that in C. albicans treatment with Micafungin, in addition to having the expected toxic antifungal effect, potentiates the immune response, improving the interaction and activation of human macrophages, probably through the unmasking of β-glucans on the cell wall surface.