Role of innate immunity in the pathogenesis of atopic dermatitis

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591659
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: KATOH Norito 京都府立医科大学, 医学(系)研究科(研究院), 教授 (30244578)
• Co-Investigator(Kenkyū-buntansha): UETA Mayumi 同志社大学, 生命医科学部, 准教授 (60398386) ; MINEOKA Risa 京都府立医科大学, 大学院医学研究科皮膚科学, 助教 (80464585)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: アトピー性皮膚炎 / 自然免疫 / 炎症

Outline of Final Research Achievements

The purpose of this project is to study the role of innate immunity in the pathogenesis of atopic dermatitis by examine the relationship between endogenous ligand and toll-like receptor. We investigated the functions of TLR3 in allergic and irritant contact dermatitis (ICD). The contact hypersensitivity (CHS) response was lower in Toll-like receptor 3 knockout (Tlr3 KO) mice, and was greater in TLR3 transgenic (Tg) mice than in wild-type (WT) mice after challenge with 2,4,6-trinitro-1-chlorobenzene. Adoptive transfer of immunized lymph node cells from Tlr3 KO mice induced CHS in WT recipients. In contrast, adoptive transfer of those from WT mice did not fully induce CHS in Tlr3 KO recipients. The ICD reaction following croton oil application was lower in Tlr3 KO mice, and was greater in TLR3 Tg mice than in WT mice. These results show that TLR3 enhances antigen-independent skin inflammation in the elicitation phase of allergic contact dermatitis and in ICD.

Free Research Field

皮膚免疫学