作者: Mathias Heikenwalder , Christian Federau , Lotta von Boehmer , Petra Schwarz , Mareike Wagner
DOI: 10.1016/J.JNEUROIM.2007.09.022
关键词:
摘要: Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases of animals and humans. Many TSEs initiated by prion replication in the lymphoreticular system (LRS). The cellular molecular prerequisites for trafficking within LRS not fully understood. Here we have manipulated CD40 its ligand to investigate whether genetic or pharmacological ablation germinal center B cells (GCBs), which migrate into out centers, influences pathogenesis. In contrast previous reports, no alteration pathogenesis was detected mice lacking CD40L treated with anti-CD40L antibodies. These results suggest that GCBs alone do impact peripheral splenic transport, efficiency, neuroinvasion, point other mechanisms affecting transport from sites nervous system.