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J. Biol. Chem., Vol. 279, Issue 53, 55493-55498, December 31, 2004

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Targeted Disruption of MAIL, a Nuclear IB Protein, Leads to Severe Atopic Dermatitis-like Disease^*

From the ^aDepartment of Veterinary Physiology, Faculty of Agriculture, Iwate University, Ueda 3-18-8, Morioka 020-8550, Japan, the ^bDepartment of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Yanagido 1-1, Gifu 501-1193, Japan, the ^cLaboratory of Anatomy, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan, the ^dUnited Graduate School of Veterinary Sciences, Gifu University, Yanagido 1-1, Gifu 501-1193, Japan, the ^eLaboratory for Immunogenomics, Research Center for Allergy and Immunology, The Institute of Physical and Chemical Research, Yokohama 230-0045, Japan, the ^fDepartment of Veterinary Science, National Institute of Infectious Diseases, Tokyo 162-8640, Japan, the ^gDepartment of Morphogenesis, Kumamoto University, Honjo 2-2-1, Kumamoto, 860-0811, Japan, the ^hCell Fate Signaling Research Unit, Discovery Research Institute, the Institute of Physical and Chemical Research, Wako, Saitama 351-0198, Japan, and the ⁱLaboratory of Cytology and Histology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan

MAIL (molecule-possessing ankyrin repeats induced by lipopolysaccharide) is a nuclear IB protein that is also termed interleukin-1-inducible nuclear ankyrin repeat protein or inhibitor of nuclear factor B (IB) . In this study, we generated Mail^–/– mice to investigate the roles of MAIL in whole organisms. Mail^–/– mice grew normally until 4–8 weeks after birth, when they began to develop lesions in the skin of the periocular region, face, and neck. MAIL mRNA and protein were constitutively expressed in the skin of wild type controls, especially in the keratinocytes. Serum IgE was higher in Mail^–/– mice than in normal. Histopathological analysis indicated that the Mail^–/– skin lesions appeared to be atopic dermatitis (AD) eczema with inflammatory cell infiltration. In addition, markedly elevated expression of some chemokines such as thymus and activation-regulated chemokine was detected in the Mail^–/– skin lesions, similar to that observed in the skin of patients with AD. In Mail^–/– mice, MAIL-deficient keratinocytes might be activated to produce chemokines and induce intraepidermal filtration of inflammatory cells, resulting in the onset of the AD-like disease. These findings suggest that MAIL is an essential molecule for homeostatic regulation of skin immunity. The Mail^–/– mouse is a valuable new animal model for research on AD.

Received for publication, August 25, 2004

^* This work was supported in part by grants-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^j To whom correspondence should be addressed: Laboratory of Cytology and Histology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan. Tel.: 81-11-706-7151; Fax: 81-11-706-7151; E-mail: mmorimat{at}med.hokudai.ac.jp.

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