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A novel hairless mouse model on an atopic dermatitis-prone genetic background generated by receptor-mediated transgenesis

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Abstract

Current mouse models for atopic dermatitis (AD) have a serious drawback, being the existence of dense hair on the body. Thus, a hairless animal model on an AD-prone genetic background will be a powerful tool to investigate the basis of and therapy for this complex disease. We applied the Toxin Receptor-mediated Cell Knockout (TRECK) method to generate a hairless transgenic (Tg) mice on the NC/Nga background, an AD-prone inbred strain. A minigene with the mouse Keratin71 (Krt71) promoter and human diphtheria toxin receptor, which intrinsically functions as the heparin-binding EGF-like growth factor, was introduced into the pronucleus of NC/Nga oocytes. Unexpectedly NCN24, one NC/Nga Tg line, showed a dominant hairless phenotype without diphtheria toxin administration. Furthermore, the atopic dermatitis-like predisposition and IgE elevation was observed in both NCN24 and the NC/Nga wildtype strain. NCN24 mice, which we have newly developed, will be useful to assess drugs for AD therapy, being able to monitor skin inflammation without shaving.

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Acknowledgments

We thank M. Saito, Y. Nishiyama, A. Sato, S. Yamada and Y. Minegishi for their support and advice. We also thank B. Loveland, A. Kumanovics and K. Fischer-Lindahl for editorial help with the manuscript. This work was supported by the Promotion of Basic Research Activities for Innovative Biosciences (PROBRAIN), and partly by Grant-in-Aid for Young Scientists (B) from the Japanese Society for the Promotion of Science (T. T.), and the Takeda Science Foundation research grant.

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Correspondence to Hiromichi Yonekawa.

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Takada, T., Shitara, H., Matsuoka, K. et al. A novel hairless mouse model on an atopic dermatitis-prone genetic background generated by receptor-mediated transgenesis. Transgenic Res 17, 1155–1162 (2008). https://doi.org/10.1007/s11248-008-9203-6

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  • DOI: https://doi.org/10.1007/s11248-008-9203-6

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