期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2001
卷号：98
期号：16
页码：9295-9299
DOI：10.1073/pnas.151242598
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Exposure of susceptible neuroblastoma N2a cells to mouse scrapie prions leads to infection, as evidenced by the continued presence of the scrapie form of the prion protein (PrPSc) and infectivity after 300 or more cell doublings. We find that exposure to phosphatidylinositol-specific phospholipase C (PIPLC) or to the monoclonal anti-prion protein (PrP) antibody 6H4 not only prevents infection of susceptible N2a cells but also cures chronically scrapie-infected cultures, as judged by the long-term abrogation of PrPSc accumulation after cessation of treatment. A nonpassaged, stationary infected culture rapidly loses PrPSc when exposed to the antibody or PIPLC, indicating that the PrPSc level is determined by steady state equilibrium between formation and degradation, and that depletion of the cellular form of PrP can interrupt the propagation of PrPSc. These findings encourage the belief that passive immunization may provide a therapeutic approach to prion disease.
