Reduced Th17 type inflammation associated with enhanced Th1, Th2 and Treg responses in a model of reactivation of congenital ocular toxoplasmosis

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Ocular toxoplasmosis (OT) is a major cause of blindness in the world. Ocular involvement is frequently seen following congenital infection. Many of these infections are quiescent but pose a life-time risk of reactivation. We previously developed a Swiss-Webster outbred mouse model for congenital toxoplasmosis by neonatal injection of Toxoplasma gondii cysts. We also used a mouse model of direct intraocular infection to show a deleterious local Th17 type response upon primary infection. However, little is known about the physiopathology of reactivation.


In the present study, we combined our two models to study reinfection into neonatally infected mice, in comparison with a primary ocular infection. Intraocular immunological determinants were studied using both BioPlex proteomic assays in aqueous humor and RT-PCR for crucial transcription factors.


We observed diminished Th17 type reaction in reinfection, compared to primary infection. In contrast, Th2 and T regulatory responses were enhanced. Interestingly, this was also true for Th1 responses, which was paralleled by a better parasite control. We observed a similar protective immune reaction pattern in the eye upon reinfection with the virulent RH strain, with the notable exception of IFN-γ.


In summary, our results show a less pathogenic but more effective anti-parasite pattern during reinfection.

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