Open Access Green as soon as Postprint is submitted to ZB.
Clinical chemistry of human FcRn transgenic mice.
Mamm. Genome 23, 259-269 (2012)
Mice genetically engineered to express human FcRn are valuable models for the evaluation of therapeutic antibodies in the context of human FcRn in vivo. However, only limited clinical chemistry information on these mouse strains is available. Thus, we have compared 30 clinical chemical parameters of C57BL/6J wild-type mice, murine FcRn-knockout mice, and two human FcRn transgenic mouse strains expressing human FcRn in the absence of murine FcRn. Since FcRn-mediated recycling prevents albumin and IgG from intracellular degradation, significant differences for both proteins were observed in the murine FcRn-knockout mice. Mice lacking FcRn show lower IgG and albumin levels compared to wild-type mice. The most prominent differences in clinical chemical parameters can be explained by secondary effects of the altered albumin levels of murine FcRn-knockout mice on liver metabolism, as similar tendencies have been observed in analbuminemic Nagase rats and hypoalbuminemic human patients, showing an overall increased liver metabolism. Both human FcRn transgenic strains show clinical chemical parameters similar to those found for wild-type mice, with the exception of endogenous IgG levels, which are greatly reduced in these mice.
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Publication type Article: Journal article
Document type Scientific Article
Keywords NAGASE ANALBUMINEMIC RATS; THERAPEUTIC ANTIBODIES; HALF-LIFE; CONGENITAL ANALBUMINEMIA; NEPHROTIC SYNDROME; IGG HOMEOSTASIS; PLASMA-PROTEINS; TOTAL CALCIUM; ALBUMIN GENE; SERUM
ISSN (print) / ISBN 0938-8990
Journal Mammalian Genome
Quellenangaben Volume: 23, Issue: 3-4, Pages: 259-269
Reviewing status Peer reviewed
Institute(s) Institute of Experimental Genetics (IEG)