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Originally published In Press as doi:10.1074/jbc.M202367200 on May 22, 2002

J. Biol. Chem., Vol. 277, Issue 31, 28038-28050, August 2, 2002
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Functional Reconstitution of Human FcRn in Madin-Darby Canine Kidney Cells Requires Co-expressed Human beta 2-Microglobulin*

Steven M. ClaypoolDagger §, Bonny L. Dickinson, Masaru Yoshida§, Wayne I. Lencer||**, and Richard S. Blumberg§||**Dagger Dagger

From the Dagger  Harvard Medical School, Program in Immunology, and § Gastroenterogy Division, Brigham and Women's Hospital, the  Gastrointestinal Cell Biology and Department of Medicine, Children's Hospital, and the || Harvard Digestive Diseases Center, Boston, Massachusetts 02115

The major histocompatibility complex class I-related neonatal Fc receptor, FcRn, assembles as a heterodimer consisting of a heavy chain and beta 2-microglobulin (beta 2m), which is essential for FcRn function. We observed that, in Madin-Darby canine kidney (MDCK) cells, the function of human FcRn in mediating the bidirectional transport of IgG was significantly increased upon co-expression of the human isoform of beta 2m. In MDCK cells, the presence of human beta 2m endowed upon human FcRn an enhanced ability to exit the endoplasmic reticulum and acquire mature carbohydrate side-chain modifications at steady state, a faster kinetics of maturation, and augmented localization at the cell surface as a mature glycoprotein able to bind IgG. Although human FcRn with immature carbohydrate side-chain modifications was capable of exhibiting pH-dependent binding of IgG, only human FcRn with mature carbohydrate side-chain modifications was detected on the cell surface. These results show that human FcRn travels to the cell surface via the normal secretory pathway and that the appropriate expression and function of human FcRn in MDCK cells depends upon the co-expression of human beta 2m.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** Supported by National Institutes of Health (NIH) Grant DK53056 and the Harvard Digestive Diseases Center.

Dagger Dagger Supported by NIH Grants DK44319 and DK51362. To whom correspondence should be addressed: Gastroenterology Division, Dept. of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St., Boston, MA 02115. Tel.: 617-732-6917; Fax: 617-264-5185; E-mail: rblumberg@partners.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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