Figure 9.

Restoration of resistance to JE by adoptive transfer of CX₃CR1⁺ DCs. CX₃CR1⁺CD11c⁺ DCs from spleens of wild-type mice were sorted and adoptively transferred into CX₃CR1^−/− mice via tail vein and foot pad inoculation (5 × 10⁵ cells/mouse). CX₃CR1^−/− recipients (n = 10–11) were subsequently infected with JEV (5.0 × 10⁷ PFU) via footpad inoculation. CX₃CR1^+/+ wild-type mice and CX₃CR1^−/− mice that received no cells were used as positive and negative controls, respectively. (A) Susceptibility of CX₃CR1^−/− recipients for CX₃CR1⁺CD11c⁺ DCs to JE. The proportion of surviving mice in each group was monitored daily for 20 days. (B) Encephalitis score. Mice infected with JEV were scored for encephalitis from 3 to 12 dpi and the encephalitis score was expressed as the average score ± SEM of each group. (C) Changes in body weight. Changes in body weight were expressed as average percentage ± SEM of body weight relative to the time of challenge. (D) Viral burden in peripheral lymphoid and CNS tissues of CX₃CR1^−/− recipients for CX₃CR1⁺CD11c⁺ DCs during JE progression. The viral burdens in spleen, brain, and spinal cord of CX₃CR1^−/− recipients infected with JEV were assessed by real-time qRT-PCR at indicated dpi. Viral RNA load was expressed as viral RNA copy number per microgram of total RNA. Data show the average ± SEM of levels derived from at least three independent experiments (n = 4–5). ^*p < 0.05; ^**p < 0.01; and ^***p < 0.001 comparing CX₃CR1^−/− mice and CX₃CR1^−/− recipients of CD11c⁺ DC at indicated dpi.