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Free Content Over-expression of the bovine FcRn in the mammary gland results in increased IgG levels in both milk and serum of transgenic mice

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The neonatal Fc receptor (FcRn) protects immunoglobulin G (IgG) from catabolism and is also responsible for IgG absorption in the neonatal small intestine. However, whether it mediates the transfer of IgG from plasma to milk still remains speculative. In the present study, we have generated transgenic mice that over-express the bovine FcRn (bFcRn) in their lactating mammary glands. Significantly increased IgG levels were observed in the sera and milk from transgenic animals, suggesting that the over-expressed bFcRn could bind and protect endogenous mouse IgG and thus extend its lifespan. We also found that injected human IgG showed a significantly longer half-life (7–8 days) in the transgenic mice than in controls (2·9 days). Altogether, the data suggested that bFcRn could bind both mouse and human IgG, showing a cross-species FcRn–IgG binding activity. However, we found no selective accumulation of endogenous mouse IgG or injected bovine IgG in the milk of the transgenic females, supporting a previous hypothesis that IgG was transported from serum to milk in an inverse correlation to its binding affinity to FcRn.
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Keywords: immunoglobulin G; neonatal Fc receptor; transgenic mice

Document Type: Research Article

Affiliations: 1: The State Key Laboratory for Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, China 2: Department of Animal Science, Agricultural Division, Jilin University, Changchun, Jilin, China 3: College of Animal Science and Technology, Hebei Agricultural University, Baoding, China 4: Department of Immunology, Faculty of Science, Eötvös Loránd University and, Immunology Research Group of the Hungarian Academy of Sciences at Eötvös, Loránd University, Budapest, Hungary 5: Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden

Publication date: November 1, 2007

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