Reduction of IgG in nonhuman primates by a peptide antagonist of the neonatal Fc receptor FcRn.

ABSTRACT: The neonatal Fc receptor FcRn provides IgG molecules with their characteristically long half-lives in vivo by protecting them from intracellular catabolism and then returning them to the extracellular space. Other investigators have demonstrated that mice lacking FcRn are protected from induction of various autoimmune diseases, presumably because of the accelerated catabolism of pathogenic IgGs in the animals. Therefore, targeting FcRn with a specific inhibitor may represent a unique approach for the treatment of autoimmune disease or other diseases where the reduction of pathogenic IgG will have a therapeutic benefit. Using phage display peptide libraries, we screened for ligands that bound to human FcRn (hFcRn) and discovered a consensus peptide sequence that binds to hFcRn and inhibits

SUBMITTER: Mezo AR 

PROVIDER: S-EPMC2268137 | biostudies-literature | 2008 Feb

REPOSITORIES: biostudies-literature