CCR7+ Dendritic Cells Are Sufficient to Recover a Defective Population of KLRG1+ T Cells in the Brain of Chronically Infected CCR7-/- Mice (MPF7P.716)

Toxoplasma gondii is a protozoan parasite that establishes a chronic infection in the brain. CCR7-/- mice are susceptible to challenge with normally avirulent strains of T. gondii, but if the mice are treated with sulfadiazine, a chronic infection is established. At this stage, equivalent numbers and proportions of parasite-specific T cells are seen in the brain of CCR7-/- and wild type mice suggesting normal priming is possible in the absence of CCR7. However, in contrast to their wild type counterparts, CCR7-/- mice fail to mount a protective response to rechallenge with a virulent strain, implying deficient effector mechanisms despite equivalent priming. Indeed, a profound defect is observed in the number and proportion of T cells expressing the effector marker KLRG1 in the brain of CCR7-/- mice. Here we present data showing that this defective effector population is restored upon transfer of CCR7+ dendritic cells at the chronic stage. We also present data on the role of transferred dendritic cells in survival upon rechallenge with the virulent RH strain. This data suggests a novel role for CCR7 during chronic T. gondii infection in guiding efficient dendritic cells interactions required to maintain effector populations of T cells in the brain.