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¹ Department of Internal Medicine, The Ohio State University, Columbus, OH 43210
² Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH 43210
³ Department of Pharmacy, The Ohio State University, Columbus, OH 43210
⁴ Department of Statistics, The Ohio State University, Columbus, OH 43210
⁵ The Jackson Laboratory, Bar Harbor, ME 04609

Address correspondence to Dr. Clark Anderson, Department of Internal Medicine, The Ohio State University, 415 HLRI, 473 West 12 Ave., Columbus, OH 43210. Phone: 614-247-7654; Fax: 614-247-7669; E-mail: anderson.48{at}osu.edu

The inverse relationship between serum albumin concentration and its half-life suggested to early workers that albumin would be protected from a catabolic fate by a receptor-mediated mechanism much like that proposed for IgG. We show here that albumin binds FcRn in a pH dependent fashion, that the lifespan of albumin is shortened in FcRn-deficient mice, and that the plasma albumin concentration of FcRn-deficient mice is less than half that of wild-type mice. These results affirm the hypothesis that the major histocompatibility complex–related Fc receptor protects albumin from degradation just as it does IgG, prolonging the half-lives of both.

Key Words: antibody • transport • half-life • pharmacokinetics • metabolism

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