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Analysis of function of CD326 expressed in dermal Dendritic cells

Research Project

Project/Area Number 16K19738
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Dermatology
Research InstitutionKeio University

Principal Investigator

OUCHI TAKESHI  慶應義塾大学, 医学部(信濃町), 助教 (30528419)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
KeywordsCD326 / ランゲリン陽性真皮樹状細胞 / ランゲルハンス細胞 / 顆粒層 / Langerin陽性真皮樹状細胞 / EpCAM / 皮膚樹状細胞
Outline of Final Research Achievements

CD326 is a membrane glycoprotein that promotes intercellular adhesion through homophilic interaction. CD326 is expressed at high levels by epidermal Langerhans Cells (LC). Here, we demonstrated that langerin+ dermal dendritic cells (langerin+ dDC) weekly express CD326 on surface. It is also found that langerin+ dDC showed enhanced expression of CD326 in lymph nodes. To study function of CD326 in langerin+ dDC, we developed KO mice in which CD326 is selectively deleted in LC and langerin+ dDC. We explored immunological consequences of lack of CD326 expression on langerin+ dDC by percutaneous immunization assays. We also found that CD326 was expressed at the second layer of stratum granulosum (SG2) layer to seal the intercellular junctions. Activated LC dendrites docking point lost CD326 expression in mice with CD326-deficient LC at SG2. Topically applied biotin penetrated into basal layer in mice with CD326-deficient LCs, suggesting the barrier compromise at LC docking points at SG2.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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