Pathogenic mechanisms of atopic dermatitis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25253071
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: Kawakami Toshiaki 国立研究開発法人理化学研究所, 統合生命医科学研究センター, チームリーダー (60143418)
• Co-Investigator(Kenkyū-buntansha): Izuhara Kenji 佐賀大学, 医学部, 教授 (00270463) ; Matsumoto Kenji 国立研究開発法人国立成育医療研究センター, 免疫アレルギー・感染研究部, 部長 (60181765)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: アトピー性皮膚炎 / マスト細胞 / Phospholipase C-β3 / Stat5 / Periostin

Outline of Final Research Achievements

Atopic dermatitis (AD) is a chronic inflammatory skin disease featured with itching and type 2 inflammation. Evidence has been accumulated showing that skin barrier impairment and immune dysregulation underlie the disease. This research project has been focused on revealing the disease pathogenesis at the cellular and molecular levels by studying murine AD models that develop skin inflammation in either a spontaneous or allergen-induced manner. So far, our data have shown that mast cells, but not basophils, are required for allergen-induced skin inflammation. Our analysis of conditional knockout mice lacking the Plcb3 gene encoding phospholipase C-β3 in various cell-specific fashions has not been completed yet. However, our data indicate that Plcb3 in CD4 T cells is not required for spontaneous development of AD-like skin inflammation in Plcb3-decifient mice.

Free Research Field

アレルギー、マスト細胞、シグナル伝達