γδ T cells induced by zoledronate under macrophage-depleted conditions reduce disease severity and parasite number in Eimeria tenella-infected chicks.

Disease severity and local immune responses mediated by Zoledronate (ZOL)-induced γδ T cells were evaluated in chicks infected with E. tenella under macrophage-depleted conditions. Three groups of White Leghorns, including a negative control group (CT), carrageenan-treated group (CAR), and both ZOL and CAR-treated group (ZOL/CAR), were infected orally with E. tenella sporulated oocysts (1 × 104 oocysts/chick) at 14 days of age. Fecal oocyst shedding was assessed at 4-15 days post-infection. The cecum was collected for histopathological and gene expression analyses. Oocyst shedding was significantly reduced in the CAR and ZOL/CAR groups compared with the CT group (p < 0.01). The total oocyst number in the ZOL/CAR group was lower compared with those in the CAR and CT groups (p < 0.05). The lesion score and parasite burden in the CAR and ZOL/CAR groups were lower compared with those in the CT group (p < 0.01). The expression of IFN-λ, IL-17 A, and perforin mRNA in the ZOL/CAR group increased compared with that in the CAR group, whereas the expression of IFN-γ in the ZOL/CAR group decreased. The results suggest that Th1-independent immunity occurs as a local immune response induced by IL-17 A/IL-22-producing γδ T cells, which control E. tenella-induced pathology in the cecum.