Identification and function of neonatal Fc receptor in mammary gland of lactating mice

TLDR

Neonatal Fc receptor (FcRn) mediates IgG transfer across the yolk sac and neonatal intestine in rodents, enabling both antenatal and milk‑borne IgG delivery, a mechanism distinct from the human transplacental route. This study examined whether FcRn regulates IgG transfer into mouse milk. FcRn was detected in functional form within mammary epithelial acini, and IgG and Fc fragment transfer was inversely related to FcRn binding affinity, indicating a recycling role that may help maintain serum IgG levels.

Abstract

In addition to its proposed function in regulating serum IgG levels, the MHC class I-related neonatal Fc receptor (FcRn) is known to play a role in IgG transfer across rodent yolk sac and neonatal intestine. In contrast to humans, for which transplacental transfer of IgG appears to be the only mechanism of maternal IgG delivery, the transmission of IgG in mice occurs both antenatally (yolk sac) and neonatally (transport from mother's milk across intestinal epithelial cells). In the current study, a possible role for FcRn in regulating IgG transfer into milk has been investigated. FcRn has been shown to be present in functional form in the mammary gland of lactating mice, and is localized to the epithelial cells of the acini. Analysis of the transfer of Fc fragments and IgG which have different affinities for FcRn indicate that, unexpectedly, these proteins are transferred in inverse correlation with their binding affinity for FcRn. Thus, in the lactating mammary gland FcRn appears to play a role in recycling IgG in a mode that may have relevance to FcRn trafficking during the maintenance of constant serum IgG levels.