Báo cáo y học: "Role of TRPV3 in immune response to development of dermatitis"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Role of TRPV3 in immune response to development of dermatitis. | Journal of Inflammation BioMed Central Research Role of TRPV3 in immune response to development of dermatitis Kinichi Imura Takeshi Yoshioka Tsutomu Hirasawa and Tsuneaki Sakata Open Access Address Discovery Research Laboratories Shionogi Co Ltd 3-1-1 Futaba-cho Toyonaka Osaka 561-0825 Japan Email Kinichi Imura - Takeshi Yoshioka - Tsutomu Hirasawa - Tsuneaki Sakata - Corresponding author Published 25 May 2009 Received 15 October 2008 Journal of Inflammation 2009 6 17 doi 1476-9255-6-17 Accepted 25 May 2009 This article is available from http content 6 1 17 2009 Imura et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Recently it has been reported that the Gly573Ser substitution of transient receptor potential V3 TRPV3 leads to increased ion-channel activity in keratinocytes. Our previous studies have indicated that the spontaneous hairless and dermatitis phenotypes of DS-Nh mice which were newly established as an animal model of atopic dermatitis AD are caused by TRPV3Gly573Ser. Although this substitution causes hairlessness in several kinds of rodents in our investigations dermatitis developed in only a few animals. Here we generated NC Nga-Nh mice to elucidate the role of TRPV3Gly573Ser in NC Nga mice which is one of the most studied animal models of AD. Methods To establish and validate the new AD animal model NC Nga-Nh mice were generated using NC Nga and DS-Nh mice and their clinical features were compared. Next T-cell receptor TCR VP usage in splenocytes evaluation of bacterial colonization and serological and histological analyses were

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