Dendritic cells (DCs) are short-lived immune cells that continuously sample antigens in the periphery, mature and migrate to the T cell zone in the lymph nodes. There they present the antigens to naïve T cells to induce either tolerance (to harmless or self-antigens) or immunity (against foreign antigens). This choice depends on how the antigen was perceived during uptake and is defined by the type of DC maturation. Our lab recently mapped the pathways leading to homeostatic DC maturation induced by uptake of apoptotic cells that entail several mechanisms to dampen the ensuing immune response. But what happens when DCs are sampling self-antigens during an infection? How do they avoid that harmless antigens will be presented in an immunogenic context due to the activation of inflammatory cascades in DCs by host-derived cytokines. This project aims to address this question by studying the pathways of DC maturation in the context of Toxoplasma gondii infection. It builds on previous observations of our lab, in which we found that DC migration to the LNs is blocked during infection. This led us to revise the concept of semi-maturation that states that there are fundamental differences between danger molecule- and host cytokine-induced DC maturation. This concept is not novel but recently developed technologies and new insights will now allow us to dissect at a molecular level the mechanisms that underly this critical checkpoint to prevent autoimmunity.