Abstract
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.
Original language | English (US) |
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Pages (from-to) | 315-322 |
Number of pages | 8 |
Journal | Journal of Experimental Medicine |
Volume | 197 |
Issue number | 3 |
DOIs | |
State | Published - Feb 3 2003 |
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology