Mapping of a gene responsible for dermatitis in NOA (Naruto Research Institute Otsuka Atrichia) mice, an animal model of allergic dermatitis

Natori, Kyoko; Tamari, Mayumi; Watanabe, Otsu; Onouchi, Yoshihiro; Shiomoto, Yasuhisa; Kubo, Shuji; Nakamura, Yusuke

doi:10.1007/s100380050181

Cited by 25 publications

(8 citation statements)

References 23 publications

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“…Although the phenotypes of both strains are controlled by polygenic traits, the major genetic determinant is located on chromosome 9 (derm1 locus) in NC (13) and on chromosome 14 in NOA (9). NOA also possesses two additional modifier genes on chromosomes 7 and 13 (14).…”

Section: Discussionmentioning

confidence: 99%

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An Atopic Dermatitis-Like Skin Disease with Hyper-IgE-emia Develops in Mice Carrying a Spontaneous Recessive Point Mutation in theTraf3ip2(Act1/CIKS) Gene

Matsushima

Kikkawa

Takada

et al. 2010

The Journal of Immunology

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Spontaneous mutant mice that showed high levels of serum IgE and an atopic dermatitis (AD)-like skin disease were found in a colony of the KOR inbred strain that was derived from Japanese wild mice. No segregation was observed between hyper-IgE-emia and dermatitis in (BALB/c × KOR mutant) N2 mice, suggesting that the mutation can be attributed to a single recessive locus, which we designated adjm (atopic dermatitis from Japanese mice). All four adjm congenic strains in different genetic backgrounds showed both hyper-IgE-emia and dermatitis, although the disease severity varied among strains. Linkage analysis using (BALB/c × KOR-adjm/adjm) N2 mice restricted the potential adjm locus to the 940 kb between D10Stm216 and D10Stm238 on chromosome 10. Sequence analysis of genes located in this region revealed that the gene AI429613, which encodes the mouse homologue of the human TNFR-associated factor 3-interacting protein 2 (TRAF3IP2) protein (formerly known as NF-κB activator 1/connection to IκB kinase and stress-activated protein kinase/Jun kinase), carried a single point mutation leading to the substitution of a stop codon for glutamine at amino acid position 214. TRAF3IP2 has been shown to function as an adaptor protein in signaling pathways mediated by the TNFR superfamily members CD40 and B cell-activating factor in epithelial cells and B cells as well as in the IL-17–mediated signaling pathway. Our results suggest that malfunction of the TRAF3IP2 protein causes hyper-IgE-emia through the CD40- and B cell-activating factor-mediated pathway in B cells and causes skin inflammation through the IL-17–mediated pathway. This study demonstrates that the TRAF3IP2 protein plays an important role in AD and suggests the protein as a therapeutic target to treat AD.

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Section: Discussionmentioning

confidence: 99%

“…Recently, two promising mouse models for human AD were described by Matsuda et al (8) and Natori et al (9). These models are represented by the inbred strains NC/Nga (NC) and Naruto Research Institute Otsuka Atrichia (NOA).…”

mentioning

confidence: 99%

An Atopic Dermatitis-Like Skin Disease with Hyper-IgE-emia Develops in Mice Carrying a Spontaneous Recessive Point Mutation in theTraf3ip2(Act1/CIKS) Gene

Matsushima

Kikkawa

Takada

et al. 2010

The Journal of Immunology

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“…NOA mice (Naruto Research Institute Otsuka Atrichia, Naruto, Japan) were of Japanese fancy-mice origin and are reported to have high susceptibility to development of atopic eczemalike dermatitis. 21 All animal experiments were performed under the protocol approved by each institutional review board. Cultured mouse MCs were generated from the femoral bone marrow cells of mice as described previously.…”

Section: Culture Of Mouse Mcs From Bone Marrow Cellsmentioning

confidence: 99%

Marked increase in CC chemokine gene expression in both human and mouse mast cell transcriptomes following Fcepsilon receptor I cross-linking: an interspecies comparison

Nakajima

Inagaki²,

Tanaka³

et al. 2002

Blood

104

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“…A genome-wide linkage analysis for susceptibility loci for atopic dermatitis in a mouse model was performed in NOA (Naruto Research Institute Otsuka Atrichia) mice [24]. The NOA mouse strain is regarded as a model for severe allergic dermatitis as the strain develops severe ulcerative skin lesions with accumulation of mast cells and significantly increased total serum IgE levels.…”

Section: Linkage Of Atopy-related Phenotypes Of the Skinmentioning

confidence: 99%

Mouse Models for the Genetic Dissection of Atopy

Heinzmann

Daser

2002

Int Arch Allergy Immunol

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Atopic disorders are complex traits with a significant contribution of heritability. Several mouse models for atopic phenotypes such as allergen-induced and intrinsic asthma, atopic dermatitis and immediate cutaneous hypersensitivity have been used to systematically dissect the genetics of these diseases. Many of the chromosomal regions identified in genome-wide screens colocalize with linkage regions of autoimmune phenotypes suggesting common regulatory genes in combination (or addition) to disease-specific genes. Moreover, many of these regions correspond to regions found in the human system, thus strengthening the likelihood of a gene contributing to the phenotype. The role of individual candidate genes has been vigorously pursued in genetically modified mice by destruction or overexpression of the candidate gene. The complex interactions of multiple contributing genes may further be elucidated in randomly mutated mouse strains. Thus mouse models can contribute largely to the elucidation of disease genes.

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Mapping of a gene responsible for dermatitis in NOA (Naruto Research Institute Otsuka Atrichia) mice, an animal model of allergic dermatitis

Cited by 25 publications

References 23 publications

An Atopic Dermatitis-Like Skin Disease with Hyper-IgE-emia Develops in Mice Carrying a Spontaneous Recessive Point Mutation in theTraf3ip2(Act1/CIKS) Gene

An Atopic Dermatitis-Like Skin Disease with Hyper-IgE-emia Develops in Mice Carrying a Spontaneous Recessive Point Mutation in theTraf3ip2(Act1/CIKS) Gene

Marked increase in CC chemokine gene expression in both human and mouse mast cell transcriptomes following Fcepsilon receptor I cross-linking: an interspecies comparison

Mouse Models for the Genetic Dissection of Atopy

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