Flaky tail mouse denotes human atopic dermatitis in the steady state and by topical application with Dermatophagoides pteronyssinus extract

Catharina Sagita Moniaga, Gyohei Egawa, Hiroshi Kawasaki, Mariko Hara-Chikuma, Tetsuya Honda, Hideaki Tanizaki, Saeko Nakajima, Atsushi Otsuka, Hiroyuki Matsuoka, Akiharu Kubo, Jun Ichi Sakabe, Yoshiki Tokura, Yoshiki Miyachi, Masayuki Amagai, Kenji Kabashima

研究成果: Article査読

89 被引用数 (Scopus)

抄録

The barrier abnormality, a loss-of-function mutation in the gene encoding filaggrin (FLG), which is linked to the incidence of atopic dermatitis (AD), is a recently discovered but important factor in the pathogenesis of AD. Flaky tail (Flgft) mice, essentially deficient in filaggrin, have been used to investigate the role of filaggrin on AD. However, the relevancy of Flg ft mice to human AD needs to be determined further. In this study, we observed the clinical manifestations of Flgft mice in the steady state and their cutaneous immune responses against external stimuli, favoring human AD. Under specific pathogen-free conditions, the majority of Flg ft mice developed clinical and histological eczematous skin lesions similar to human AD with outside-to-inside skin barrier dysfunction evaluated by newly devised methods. In addition, cutaneous hapten-induced contact hypersensitivity as a model of acquired immune response and a mite extract-induced dermatitis model physiologically relevant to a human AD were enhanced in Flgft mice. These results suggest that the Flg ft mouse genotype has potential as an animal model of AD corresponding with filaggrin mutation in human AD.

本文言語English
ページ(範囲)2385-2393
ページ数9
ジャーナルAmerican Journal of Pathology
176
5
DOI
出版ステータスPublished - 2010 5

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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