XXXX driven inflammatory response induces retinal pathology in a model of @entity17577 reactivation.

@entity1 @entity32 @entity19 @entity61 @entity17577 @entity281 @entity777 @entity69132 @entity989 @entity636 @entity630 @entity3204
UNASSIGNED: @entity32 is one of the consequences of infection with the protozoan parasite @entity3204 . Even if lesions are self-healing in immunocompetent @entity1 , they pose a life-time risk of reactivation and are a serious threat to vision. As there are virtually no immunological data on reactivating @entity17577 , we established a model of direct intravitreal injection of parasites in previously infected @entity19 with a homologous type II strain. Two different @entity19 strains with variable ability to control @entity989 were studied in order to describe protective and deleterious reaction patterns. In Swiss-Webster @entity19 , which are already relatively resistant to @entity281 , no peak of parasite load was observed upon reinfection. In contrast, the susceptible inbred strain C57Bl/6 showed high parasite loads after 7 days, as well as marked deterioration of retinal architecture. Both parameters were back to normal at day 21. C57Bl/6 @entity19 also reacted with a strong local production of inflammatory and @entity630 type cytokines like @entity777 , @entity636 and IFN-y, while Swiss-Webster @entity19 only showed moderate expression of the @entity61 cytokine @entity69132 . Interestingly, rapid intraocular production of anti- @entity3204 antibodies was observed in Swiss-Webster, but not C57Bl/6 @entity19 . We then localized the cellular source of different immune mediators within the retina by immunofluorescence. Finally, neutralization experiments of IFN-y or @entity777 demonstrated the respective protective and deleterious roles of these cytokines for parasite control and retinal integrity during reinfection. In conclusion, we developed and immunologically characterized a promising @entity19 model of reactivating @entity17577 .
