A primary infection with the coccidian protozoan Toxoplasma gondii, responsible for toxoplasmosis, induces in an immunocompetent individual a immune response which usually limits the replication of the invasive form of T. gondii, resulting in the formation of the dormant stage of the parasite. Because of this effective immune reaction, the chronic infection results in protective immunity, which is thought to mainly involve a systemic Th1 response focused on IL-12 secreted by dendritic cells (DCs) and interferon-gamma production by CD4⁺ and CD8⁺ T lymphocytes. DCs are now recognized as key elements for development of immunity against Toxoplasma, due to their ability to acquire toxoplasma antigens, migrate from peripheral tissues to lymphoid organs, deliver information to naive T cells, and secrete immune-polarizing cytokines such as IL-12. Dendritic cells have a critical importance of as a first line of defense in controlling T. gondii. In addition to their role in initiation of immunity to Toxoplasma, there is evidence that DCs serve as vehicles for dissemination during infection. Toxoplasma is able to influence and regulate dendritic cell function and motility and exploits DCs as Trojan horses, targeting them for early infection, suppressing their cytokine effector function, and using them for dissemination within the host with an impact on the outcome of disease. T. gondii  is a supreme manipulator of the immune response so that immunity to T. gondii is a delicate balance between the parasite and its host involving a coordinated series of DC interactions.