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Localization of the site of the IgG molecule that regulates maternofetal transmission in mice

Localization of the site of the IgG molecule that regulates maternofetal transmission in mice Site‐directed mutagenesis of a recombinant Fc hinge fragment has recently been used to localize the site of the mouse IgG1 (mIgG1) molecule that is involved in the intestinal transfer of recombinant Fc hinge fragments in neonatal mice. This site encompasses Ile‐253, His‐310, Gln‐311, His‐433 and Asn‐434, localized at the CH2‐CH3 domain interface and overlapping with the staphylococcal protein A‐binding and catabolic sites. In the present study, the effect of these mutations on the maternofetal transfer of Fc hinge fragments has been studied. Experiments to analyze transfer of radiolabeled Fc hinge fragments from the circulation of 15–18 day pregnant mice to fetuses in utero demonstrate that the mutations affect the maternofetal transmission in a way that correlates closely with the effects of the mutations on intestinal transfer and catabolism. The studies indicate that the neonatal Fc receptor, FcRn, is involved in transcytosis across both yolk sac and neonatal intestine in addition to the regulation of IgG catabolism. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Immunology Wiley

Localization of the site of the IgG molecule that regulates maternofetal transmission in mice

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References (22)

Publisher
Wiley
Copyright
Copyright © 1996 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
ISSN
0014-2980
eISSN
1521-4141
DOI
10.1002/eji.1830261038
pmid
8898970
Publisher site
See Article on Publisher Site

Abstract

Site‐directed mutagenesis of a recombinant Fc hinge fragment has recently been used to localize the site of the mouse IgG1 (mIgG1) molecule that is involved in the intestinal transfer of recombinant Fc hinge fragments in neonatal mice. This site encompasses Ile‐253, His‐310, Gln‐311, His‐433 and Asn‐434, localized at the CH2‐CH3 domain interface and overlapping with the staphylococcal protein A‐binding and catabolic sites. In the present study, the effect of these mutations on the maternofetal transfer of Fc hinge fragments has been studied. Experiments to analyze transfer of radiolabeled Fc hinge fragments from the circulation of 15–18 day pregnant mice to fetuses in utero demonstrate that the mutations affect the maternofetal transmission in a way that correlates closely with the effects of the mutations on intestinal transfer and catabolism. The studies indicate that the neonatal Fc receptor, FcRn, is involved in transcytosis across both yolk sac and neonatal intestine in addition to the regulation of IgG catabolism.

Journal

European Journal of Immunology – Wiley

Published: Oct 1, 1996

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