In parallel to the increased intracerebral load, even the production of antiparasitic IGTP and iNOS as well as IL-1β and IL-18 was increased in CD11c-Cre OTUB1fl/fl mice (Supplementary Fig. 5j), further indicating that the aggravated course of TE in CD11c-Cre OTUB1fl/fl mice was caused by an impaired DC immune response early after infection but not by an insufficient intracerebral immune response. This evidence concerns the gene NOS2 and infection.