**3. Conclusion**

Four promising mouse models for human AD have been established thus far in Japan. Two models are polygenic, and the pathology and the onset of the disease are very similar to

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human AD, although no responsible genes have been isolated. In contrast, the other two models are monogenic, and the responsible genes have been identified. One, DS-*Nh*, is a gain-of-function mutation in the *Trpv3* locus, whereas the other, KOR-*adjm*, is a loss-offunction mutation in the *Traf3ip2* locus. The former mutation demonstrated the strong involvement of IL-13 in association with the *Trpv3* locus and the TCRV<sup>b</sup> (NKT cell) haplotype. The latter mutation demonstrated the involvement of CD40L/BAFF signaling for B cell activation and of the IL-17 signaling pathway for the autoimmune and inflammatory responses through the activation of NF-B. The involvement of the NF-B pathway to AD is commonly suggested in both human and mouse, and therefore the finding shown here will facilitate the development of therapies and drugs.
