期刊
JOURNAL OF VIROLOGY
卷 81, 期 9, 页码 4877-4880出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02345-06
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Controversial results have been observed in mouse models regarding the role of lymphoid tissues in prion pathogenesis. To investigate the role of dendritic cells (DC), we used a transgenic mouse model. In this model (CD11c-N17Rac1), a significant reduction of CD8(+) CD11c(hi)DC has been described, and the remaining CD8(+) DC demonstrate a reduced capacity for the uptake of apoptotic cells. After intraperitoneal prion infection, significantly longer incubation times were observed in CD11c-N17Rac1 mice than in controls, indicating that a defect in CD8(+) CD11c(hi) DC significantly impedes neuroinvasion after intraperitoneal infection. In contrast, no distinct differences were observed between CD11c-N17Rac1 mice and controls after oral infection. This provides evidence that oral and intraperitoneal prion infections differ in lymphoreticular requirements.
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