Roles of connective tissue fibroblasts in the pathogenesis of atopic dermatitis

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860765
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: ANDO Tomoaki 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, 研究員 (10724669)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: アトピー性皮膚炎 / 線維芽細胞 / PLC-beta3 / SPS複合体

Outline of Final Research Achievements

We investigated the mechanisms underlying hyper-expression of Periostin in phospholipase C (PLC)-beta3 deficient fibroblasts. In addition, we examined the in vitro effects of PLC-beta3 supplement therapy. Stimulation by IL-13, which is known to activate Periostin production, induced hyper phosphorylation of both Stat5 and Stat6 in PLC-beta3 deficient fibroblasts. On the other hand, transfection of fibroblasts with fusion proteins of PLC-beta3 fragment and SHP-1 suppressed the activation of Stat5 and Stat6. These results would serve as a basis for developing new therapeutics for the atopic dermatitis targeting SHP-1-PLC-beta3-Stat5 (SPS) complex.

Free Research Field

アレルギー学