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FcRn in the Yolk Sac Endoderm of Mouse Is Required for IgG Transport to Fetus¹

Jonghan Kim^2,*,, Sudhasri Mohanty^2,*, Latha P. Ganesan^*, Keding Hua, David Jarjoura, William L. Hayton, John M. Robinson and Clark L. Anderson^3,*

^* Department of Internal Medicine, College of Pharmacy, Center for Biostatistics, and Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH 43210

In adults, the nonclassical MHC class I molecule, FcRn, binds both IgG and albumin and rescues both from a degradative fate, endowing both proteins with high plasma concentrations. FcRn also transports IgG from mother to young during gestation. Anticipating that a detailed understanding of gestational IgG transport in the mouse may give us a useful model to understand FcRn function in the human placenta, we have studied FcRn in the mouse yolk sac placenta in detail. Analyzing day 19–20 fetuses of the three FcRn genotypes resulting from matings of FcRn^+/– parents, we found that FcRn^–/– fetuses showed negligible IgG concentrations (1.5 µg/ml), whereas IgG concentrations in FcRn^+/– fetuses were about a half (176 µg/ml) that of FcRn^+/+ fetuses (336 µg/ml), indicating that FcRn is responsible for virtually all IgG transport from mother to fetus. Immunofluorescence and immunoblotting studies indicated that FcRn is expressed in the endoderm of the yolk sac placenta but not in other cells of the yolk sac placenta or in the chorioallantoic placenta. IgG was found in the endoderm of both FcRn^+/+ and FcRn^–/– yolk sac placentas and in the mesenchyme of FcRn^+/+ but was missing from the mesenchyme of FcRn^–/– yolk sac placentas, indicating that IgG enters the endoderm constitutively but is moved out of the endoderm by FcRn. The similarities of these results to human placental FcRn expression and function are striking.

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

¹ This work was supported in part by Grants HD38764, CA88053, and AI57530 from the National Institutes of Health.

² These authors contributed equally.

³ Address correspondence and reprint requests to Dr. Clark L. Anderson, Department of Internal Medicine, The Ohio State University, 012K Davis Heart and Lung Research Institute, 473 West 12th Avenue, Columbus, OH 43210. E-mail address: anderson.48{at}osu.edu

⁴ Abbreviations used in this paper: FcRn, Fc receptor (neonatal); placenta, mouse chorioallantoic placenta or the human placenta; yolk sac, mouse yolk sac placenta; CAV1, caveolin 1; DAPI, 4',6-diamidino-2-phenylindole; DIC, differential interference contrast.