Analyses for persistent inflammation in the skin and oral mucosa

2015 Fiscal Year Final Research Report

• Project/Area Number: 25670795
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Pathobiological dentistry/Dental radiology
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Azuma Miyuki 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (90255654)
• Co-Investigator(Kenkyū-buntansha): OHNO Tatsukuni 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (80435635) ; TUSHIMA Humihiko 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (90456210)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 歯学 / 免疫学 / 慢性炎症 / 口腔粘膜 / IL-33 / 免疫抑制分子 / VISTA

Outline of Final Research Achievements

Oral mucosa induced a rapid destruction of epithelium and severe infiltration, however, this recovered quickly. Impaired generation of effector T cells and increment of regulatory T cells (Tregs) in the secondary lymphoid tissues may contribute to rapid tissue repair by suppressive mechanisms of T cell activation. Our results in a happen-induced contact hypersensitivity model indicate that a novel coinhibitory molecule VISTA functions regulatory in the induction phase of T cell activation, but not at the effector phase. Although IL-33 acts as an alarmin in both innate and adaptive immunity, Il-33 is also involved in generation, activation, and recruitment of Tregs. These opposite actions disrupt the final outcome in skin and mucosal inflammation.

Free Research Field

歯学