| 摘要 |
<p>NadA, App and ORF40 function as adhesins in N.meningitidis. Adhesion can be modulated by targeting these three proteins. NadA allelic variants are disclosed. Autoproteolytic cleavage of App is disclosed, as is removal of the activity by mutagenesis. App is processed and secreted into culture medium when expressed in E.coli. Mature App proteins are disclosed. Knockout mutants are disclosed. Vesicles from non-Neisserial hosts with heterologous adhesin expression are disclosed.</p> |
