Impact of <scp>TRPV</scp>3 on the development of allergic dermatitis as a dendritic cell modulator
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- Erika Yamamoto‐Kasai
- Department of Biology Graduate School of Science Kobe University Kobe Japan
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- Kiyoshi Yasui
- Shionogi Medicinal Research Laboratories Shionogi & Co., Ltd. Osaka Japan
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- Michitaka Shichijo
- Shionogi Medicinal Research Laboratories Shionogi & Co., Ltd. Osaka Japan
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- Tsuneaki Sakata
- Department of Biology Graduate School of Science Kobe University Kobe Japan
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- Takeshi Yoshioka
- Shionogi Medicinal Research Laboratories Shionogi & Co., Ltd. Osaka Japan
Bibliographic Information
- Published
- 2013-11-27
- Rights Information
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- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
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- 10.1111/exd.12273
- Publisher
- Wiley
Search this article
Description
<jats:title>Abstract</jats:title><jats:p>The transient receptor potential channel vanilloid subfamily V member 3 (<jats:styled-content style="fixed-case">TRPV</jats:styled-content>3), which functions as a thermosensor in keratinocytes, plays an important role in the development of allergic and itchy dermatitis in rodents. Although real‐time <jats:styled-content style="fixed-case">PCR</jats:styled-content> analysis using lesional and non‐lesional skin samples from patients with atopic dermatitis showed that <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3 was expressed in lesional skin, the role that <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3 plays in patients with dermatitis is still relatively obscure. Here, we determined whether <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3 was a dendritic cell (<jats:styled-content style="fixed-case">DC</jats:styled-content>) modulator using <jats:styled-content style="fixed-case">DS</jats:styled-content>‐Nh mice with a gain‐of‐function mutation in <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3 (<jats:styled-content style="fixed-case">TRPV</jats:styled-content>3Gly573Ser), because increasing skin temperature is associated with the modulation of dermal dendritic cells (<jats:styled-content style="fixed-case">DC</jats:styled-content>s). Interestingly, increased responses to haptens by skin and <jats:styled-content style="fixed-case">DC</jats:styled-content>s were observed in <jats:styled-content style="fixed-case">DS</jats:styled-content>‐<jats:italic>Nh</jats:italic> mice compared with those from <jats:styled-content style="fixed-case">DS</jats:styled-content> mice with wild‐type <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3. Increased thymic stromal lymphopoietin (<jats:styled-content style="fixed-case">TSLP</jats:styled-content>) responses were also observed in keratinocytes from <jats:styled-content style="fixed-case">DS</jats:styled-content>‐<jats:italic>Nh</jats:italic> mice compared with those from <jats:styled-content style="fixed-case">DS</jats:styled-content> mice. Taken together, we propose that the <jats:styled-content style="fixed-case">DS</jats:styled-content>‐<jats:italic>Nh</jats:italic> mouse is a good model to use in order to better understand the role of this orphan channel and that <jats:styled-content style="fixed-case">TRPV</jats:styled-content>3 may represent a new therapeutic target in certain types of dermatitis through the control of <jats:styled-content style="fixed-case">DC</jats:styled-content>s.</jats:p>
Journal
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- Experimental Dermatology
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Experimental Dermatology 22 (12), 820-824, 2013-11-27
Wiley