Our group is involved in the analysis of host-pathogen interactions during fungal infection. We mainly use Candida albicans as model organism to explore fungal pathogenesis. Our work mainly focuses on the role that MAP kinase signal transduction pathways play in this microbe. We are interested determining the specificity of the stimuli, the responses generated and the interactions among these routes as well as the consequences of their activation. A better understanding of this complex system may be exploited for the design of new and novel antifungals. Experimental approaches and methodologies used in our research comprise molecular genetics, biochemistry, cell biology, genome wide strategies (transcriptomal and proteomic) and experimental infection in mice. Recently, we are using genetically modified strains disrupted in genes essential to pathogenesis to understand the mechanisms used by the immune system to control Candida infections. We are determining the key components (receptors and/or cytokines) that influence the decision of the host towards control (commensalism) or susceptibility to invasion (disease). We are also using model of commensalism in mice to define the role of certain host specific genes in susceptibility to infection. An envisioned short term goal of our group is to develop tools, strategies and methodologies to image in vivo a fungal infection.