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Transgenic Res. 2008 Dec;17(6):1155-62. doi: 10.1007/s11248-008-9203-6. Epub 2008 Aug 7.

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

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Department of Laboratory Animal Science, The Tokyo Metropolitan Institute of Medical Science (Rinshoken), 3-18-22, Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan.


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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